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Step 1 First Aid - Neurology

Terms in this set (564)

CNS/PNS origins: Neuroectoderm (gives rise to what?)

CNS neurons Ependymal cells (inner lining of ventricles, make CSF) Oligodendrocytes Astrocytes

CNS/PNS origins: Neural Crest (gives rise to what?)

Schwann cells PNS neurons

CNS/PNS origins: Mesoderm (gives rise to what?)

M icroglia, like M acrophages, originate from M esoderm

Neurons

Comprise nervous system. Permanent cells -- do not divide in adulthood. Large cells w/ prominent nucleoli.

Nissl substance

RER found in cell body and dendrites, but not axon of neurons.

Astrocytes

Physical support, repair, K+ metabolism, removal of excess NT. Maintenance of BBB. Reactive gliosis in response to injury. <img src="392a Astrocyte.JPG" />

Astrocyte marker?

GFAP

Microglia

CNS phagocytes. Mesodermal origin. Not readily discernible in Nissle stains. Have small, irregular nuclei and relatively little cytoplasm. <img src="392b Microglia.JPG" />

What happens to microglia in the presence of tissue damage?

Microglia --(tissue damage)--< large ameboid phagocytic cells

What happens to HIV-infected microglia?

HIV-infected microglia fuse to form multinucleated giant cells in the CNS

Oligodendria

Each oligodendrocyte myelinates multiple CNS axons (up to 30 each). In Nissle stains, they appear as small nuclei with dark chromatin and little cytoplasm. <img src="392c oligodendroglia.JPG" />

What is the predominant type of glial cell in white matter?

Oligodendrocytes.

What cells are destroyed in multiple sclerosis?

Oligodendrocytes.

What do oligodendrocytes look like on H&E?

"Fried Eggs" <img src="555a oligodendrocytes.JPG" />

Schwann cells

Each Schwann cell myelinates only 1 PNS axon. Also promote axonal regeneration. Derived from neural crest.

What are the cells that are destroyed in Guillain-Barré syndrome?

Schwann cells.

An acoustic neuroma is a type of...? Where is it located?

Acoustic neuroma is a type of Schwannoma. It is typically located in internal acoustic meatus (CN VIII)

Sensory receptors/corpuscles: Free nerve endings (C, A-delta fibers) Location? Senses?

In all skin, epidermis, some viscera. Senses pain and temperature.

Sensory receptors/corpuscles (location and senses): In all skin, epidermis, some viscera. Senses pain and temperature. Which is this?

Free nerve endings (C, A-delta fibers)

Sensory receptors/corpuscles: Meissner's corpuscles Location? Senses?

In glabrous (hairless) skin. Senses dynamic fine touch (e.g., manipulation), adapt quickly.

Sensory receptors/corpuscles (location and senses): In glabrous (hairless) skin. Senses dynamic fine touch (e.g., manipulation), adapt quickly. Which is this?

Meissner's corpuscles

Sensory receptors/corpuscles: Pacinian corpuscles Location? Senses?

In deep skin layers, ligaments, and joints. Sense vibration, pressure.

Sensory receptors/corpuscles (location and senses): In deep skin layers, ligaments, and joints. Sense vibration, pressure. Which is this?

Pacinian corpuscles

Sensory receptors/corpuscles: Merkel's disks Location? Senses?

(cup-shaped, unencapsulated) Finger tips, superficial skin. In hair follicles. Sense pressure, static touch (e.g., shapes, edges, textures), adapt slowly.

Sensory receptors/corpuscles (location and senses): (cup-shaped, unencapsulated) Finger tips, superficial skin. In hair follicles. Sense static touch (e.g., shapes, edges, textures), adapt slowly. Which is this?

Merkel's disks

Sensory receptors/corpuscles: Ruffini corpuscles Location? Senses?

Finger tips, joints. Sense pressure, slippage of objects along surface of skin, joint angle change. Adapts slowly.

Sensory receptors/corpuscles (location and senses): Finger tips, joints. Sense pressure, slippage of objects along surface of skin, joint angle change. Adapt slowly. Which is this?

Ruffini corpuscles

Peripheral nerve layers: Endoneurium

Invests a single nerve fiber (Endo = inner) <img src="393e Peripheral nerve layers.JPG" />

Peripheral nerve layers: Perineurium

(P erineurium is the P ermeability barrier) Surrounds a fascicle of nerve fibers. (Peri = around) Must be rejoined in microsurgery for limb reattachment. <img src="393e Peripheral nerve layers.JPG" />

Peripheral nerve layers: Epineurium

Dense connective tissue that surrounds entire nerve (fasicles and blood vessels) (Epi = outer) <img src="393e Peripheral nerve layers.JPG" />

Neurotransmitters: NE Change in dz? Location of synthesis?

Increased in anxiety, decreased in depression. Made in the locus ceruleus.

Increased in anxiety, decreased in depression. Made in the locus ceruleus. What NT is this?

Neurotransmitters: Dopamine Change in dz? Location of synthesis?

Increased in schizophrenia, decreased in Parkinson's. Made in the ventral tegmentum and SNc

Increased in schizophrenia, decreased in Parkinson's. Made in the ventral tegmentum and SNc What NT is this?

Dopamine

Neurotransmitters: 5-HT Change in dz? Location of synthesis?

Decreased in anxiety, depression. Made in the raphe nucleus

Decreased in anxiety, depression. Made in the raphe nucleus What NT is this?

5-HT

Neurotransmitters: ACh Change in dz? Location of synthesis?

Decreased in Alzheimer's, Huntington's. Made in the basal nucleus of Meynert.

Decreased in Alzheimer's, Huntington's. Made in the basal nucleus of Meynert. What NT is this?

ACh

What 3 structures form the blood-brain barrier (BBB)?

1.) Tight junctions btw nonfenestrated capillary endothelial cells 2.) Basement membrane 3.) Astrocyte processes <img src="394a BBB.JPG" />

Besides the BBB, what are 2 similar barriers?

1.) Blood-testis barrier 2.) Maternal-fetal blood barrier of placenta

What happens at the BBB w/ infarction?

Infarction destroys endothelial cell tight junctions, leading to vasogenic edema

Glucose and amino acids at the BBB

Cross slowly by carrier-mediated transport mechanism.

Nonpolar/lipid-soluble substances at the BBB

Cross rapidly via diffusion.

Specialized brain regions w/ fenestrated capillaries and no BBB

Allow molecules in the blood to affect brain function (e.g., area postrema - vomiting center after chemo, OVLT - osmotic sensing) or neurosecretory products to enter circulation (e.g., neurohypophysis - ADH release)

Hypothalamus functions

The hypothalamus wears TAN HATS : T hirst and water balance A denohypophysis control N eurohypophysis releases hormones from hypothalamus H unger A utonomic regulation T emperature regulation S exual urges

Inputs to the hypothalamus

OVLT (senses change in osmolarity) Area postrema (responds to emetics)

Supraoptic nucleus of the hypothalamus

Area that makes ADH.

Supraoptic nucleus of the hypothalamus

Paraventricular nucleus of the hypothalamus

Area that makes oxytocin.

Paraventricular nucleus of the hypothalamus

Lateral area of the hypothalamus

Controls hunger: destruction leads to anorexia. ("If you zap the lateral nucleus, you shrink laterally ") Inhibited by leptin.

Ventromedial area of the hypothalamus

Controls satiety: destruction leads to hyperphagia. ("If you zap your ventromedial nucleus, you grow ventrally and medially .") Stimulated by leptin.

Anterior hypothalamus

Cooling (Anterior = cooling, or A/C). A nterior is pA rasympathetic.

Posterior hypothalamus

Heating (posterior = get fired up / heating). Sympathetic. If you zap your P osterior hypothalamus, you become a P oikilotherm (cold-blooded, like a snake)

Septal nucleus of the hypothalamus

area responsible for sexual urges

Septal nucleus of the hypothalamus

Suprachiasmatic nucleus of the hypothalamus

Circadian rhythm. ("You need to sleep to be charismatic [chiasmatic]").

Posterior pituitary (neurohypophysis)

Receives hypothalamic axonal projections from supraoptic (ADH) and paraventricular (oxytocin) nuclei. Oxytocin: oxys = quick; tocos = birth.

Anterior pituitary aka...?

A nterior pituitary = A denohypophysis

Thalamus

Major relay for ascending sensory information that ultimately reaches the cortex. <img src="395a Thalamus.JPG" />

Blood supply to the thalamus

posterior communicating, posterior cerebral, and anterior choroidal arteries.

Lateral geniculate nucleus (LGN) of thalamus <img src="395b Thalamus without labels.JPG" />

(hint: "L ateral for L ight") area of thalamus for visual information.

area of thalamus for visual information.

Lateral geniculate nucleus (LGN) of thalamus <img src="395b Thalamus without labels.JPG" /> (hint: "L ateral for L ight")

Medial geniculate nucleus (MGN) of the thalamus <img src="395b Thalamus without labels.JPG" />

(hint: M edial for M usic) Area of the thalamus responsible for auditory information

Area of the thalamus responsible for auditory information

Medial geniculate nucleus (MGN) of the thalamus <img src="395b Thalamus without labels.JPG" /> (hint: M edial for M usic)

Ventral posterior nucleus, lateral part (VPL) -- of thalamus <img src="395b Thalamus without labels.JPG" />

part of the thalamus responsible for body sensation (proprioception, pressure, pain, touch, vibration via dorsal columns, spinothalamic tract).

Ventral posterior nucleus, lateral part (VPL) -- of thalamus <img src="395b Thalamus without labels.JPG" />

Ventral posterior nucleus, medial part (VPM) -- of the thalamus <img src="395b Thalamus without labels.JPG" />

(hint: you put M akeup on your face, and sensory info is relayed through the VPM ) Area of thalamus responsible for facial sensation (via CN V)

Area of thalamus responsible for facial sensation (via CN V)

Ventral posterior nucleus, medial part (VPM) -- of the thalamus <img src="395b Thalamus without labels.JPG" /> (hint: you put M akeup on your face, and sensory info is relayed through the VPM )

Motor and sensory locations in the thalamus

Motor is anterior to sensation in the thalamus, just like the cortex. <img src="395a Thalamus.JPG" />

Limbic system: Includes what? Responsible for what?

Includes cingulate gyrus, hippocampus, fornix, and mammillary bodies. Responsible for F eeding, F leeing, F ighting, F eeling, and sex (....) (The famous 5 F's )

Input to the cerebellum

Receives contralateral cortical input via middle cerebellar peduncle and ipsilateral proprioceptive information via inferior cerebellar peduncle. Input nerves = climbing and mossy fibers.

Output from the cerebellum

Provides stimulatory feedback to contralateral cortex to modulate movement. Output nerves = Purkinje fibers output deep to nuclei of cerebellum, which in turn output to cortex via superior cerebellar peduncle.

Deep nuclei of the cerebellum

Lateral to medial: D entate, E mboliform, G lobose, F astigial ("D on't E at G reasy F oods")

Lateral cerebellum

area of the cerebellum responsible for voluntary movement of extremities

Lateral cerebellum

Medial cerebellum

Area of cerebellum responsible for balance, truncal coordination.

Medial cerebellum

Basal ganglia (overall function)

Important in voluntary movements and making postural adjustments. Receives cortical input, provides negative feedback to cortex to modulate movement.

Basal ganglia (overall function)

Excitatory pathway of the basal ganglia

Substantia Nigra pars compacta's (SNc's) dopamine binds to D1 receptros in the excitatory pathway, stimulating the excitatory pathway (incr motion). Therefore, loss of dopamine in Parkinson's inhibits the excitatory pathway (decr motion). <img src="396a Excitatory and inhibitory pathways.JPG" /> Key: Grey = stimulatory || Black = inhibitory SNc = Substantia nigra pars compacta GPe = Globus pallidus externus GPi = Globus pallidus internus STN = Subthalamaic nucleus D1 = Dopamine D1 receptor (excitatory) D2 = Dopamine D2 receptor (inhibitory)

Inhibitory pathway of the basal ganglia

SNc's dopamine binds to D2 receptros in the inhibitory pathway, inhibiting the inhibitory pathway (incr motion). Therefore, loss of dopamine in Parkinson's dz excites (i.e., disinhibits) the inhibitory pathway (decr motion). <img src="396a Excitatory and inhibitory pathways.JPG" /> Key: Grey = stimulatory || Black = inhibitory SNc = Substantia nigra pars compacta GPe = Globus pallidus externus GPi = Globus pallidus internus STN = Subthalamaic nucleus D1 = Dopamine D1 receptor (excitatory) D2 = Dopamine D2 receptor (inhibitory)

Parkinson's disease

Degenerative disorder of CNS associated w/ Lewy bodies (composed of alpha-synuclein) and depigmentation of the substantia nigra pars compacta (loss of dopaminergic neurons). Rare cases have been linked to exposure to MPTP, a contaminant in illicit street drugs. ("TRaP = T remor (at rest), cogwheel R igidity, a nd P ostural instability. You are TRaP ped inside your body.")

Parkinson's disease

Hemiballismus

Sudden, wild flailing of 1 arm. Characteristic of contralateral subthalamic nucleus lesion. Loss of inhibition of thalamus through globus pallidus. ("Hemiballismus = Half ballistic -- like throwing a baseball")

Huntington's dz

Autosomal-dominant trinucleotide repeat d/o. Chromosome 4. Atrophy of caudate nucleus (loss of GABAergic neurons) leads to enlarged lateral ventricles on CT. <img src="397a HD-Atrophy of caudate nucleus.JPG" /> Chorea, depression, progressive dementia. Sx manifest in affeccted indvls btw ages 20-50. (Expansion of CAG repeats: "C audate loses A Ch and G ABA")

Huntington's dz

Chorea

Sudden, jerky, purposeless movements. Characteristic of basal ganglia lesion (e.g., Huntington's disease) (Chorea = dancing (Greek). Think choral dancing or choreography)

Athetosis

Slow, writhing movements, especially if fiingers. Characteristic of basal ganglia lesion (e.g., Huntington's dz) (Athetos = not fixed (Greek). Think snakelike.)

Essential/postural tremor

Action tremor, autosomal dominant. Essential tremor pts often self-medicate w/ alcohol, which decreases the tremor. Tx: beta-blockers.

Resting tremor

Not noticeable distally. Seen in Parkinson's ("pill-rolling" tremor)

Intention tremor

Slow, zigzag motion when pointing twd a target; associated w/ cerebellar dysfunction.

Cerebral cortex: where are the Sylvian fissure vs. Central sulcus?

A: Sylvian fissure is above temporal lobe; central sulcus divides frontal and parietal lobes. <img src="398a Cerebral cortex fxns.JPG" />

Cerebral cortex: What is the arcuate fasciculus?

Connection between Associative auditory cortex (Wernicke's area; dominant hemisphere) and Motor speech area (Broca's area; dominant hemisphere) <img src="398a Cerebral cortex fxns.JPG" />

Cerebral cortex: Where is the primary auditory cortex (Heschel's gyrus)? The primary motor area? The primary sensory area? The premotor area (part of extrapyramidal circuit)?

Frontal lobe functions

"Executive functions" Planning, inhibition, concentration, orientation, language, abstraction, judgment, motor regulation, mood. Lack of social judgment is most notable in frontal lobe lesion. ("D amage = D isinhibition" - e.g., Phineas Gage)

Homonculus: What is it? What is it used for? What reaches into the Sylvian fissure? The longitudinal fissure?

Topographical representation of sensory and motor areas in the cerebral cortex. Used to localize lesion (e.g., in blood supply) leading to specific defects. For example, lower extremity deficit in sensation or movement indicates involvement of anterior cerebral artery. <img src="399a Motor homonculus.JPG" />

Brain lesion in: Broca's area

(hint: BRO ca's is BRO ken speech.) Consequence: Motor (nonfluent/expressive) aphasia w/ good comprehension.

Motor (nonfluent/expressive) aphasia w/ good comprehension. Where is the lesion?

Broca's area (hint: BRO ca's is BRO ken speech.)

Brain lesion in: Wernicke's area

(hint: W ernicke's is W ordy but makes no sense.) Consequence: Sensory (fluent/receptive) aphasia w/ poor comprehension, neologisms.

Sensory (fluent/receptive) aphasia w/ poor comprehension, neologisms. Where is the lesion?

Wernicke's area (hint: W ernicke's is W ordy but makes no sense.)

Brain lesion in: Arcuate fasciculus (connects Wernicke's to Broca's area)

Consequence: Conduction aphasia; good comprehension, fluent speech, but poor repitition.

Conduction aphasia; good comprehension, fluent speech, but poor repitition. Where is the lesion?

Arcuate fasciculus (connects Wernicke's to Broca's area)

Brain lesion in: Amygdala (bilateral)

Consequence: Kluver-Bucy syndrome (hyperorality, hypersexuality, disinhibited behavior)

Kluver-Bucy syndrome (hyperorality, hypersexuality, disinhibited behavior) Where is the lesion?

Amygdala (bilateral)

Brain lesion in: Frontal lobe

Consequence: Personality changes and deficits in concentration, orientation, and judgment; may havve reemergence of primitive reflexes.

Personality changes and deficits in concentration, orientation, and judgment; may havve reemergence of primitive reflexes. Where is the lesion?

Frontal lobe

Brain lesion in: Right parietal lobe

Consequence: Spatial neglect syndrome (agnosia of the contralateral side of the world)

Spatial neglect syndrome (agnosia of the contralateral side of the world) Where is the lesion?

Right parietal lobe

Brain lesion in: Reticular activating system (midbrain)

Consequence: Reduced levels of arousal and wakefulness (e.g., coma)

Reduced levels of arousal and wakefulness (e.g., coma) Where is the lesion?

Reticular activating system (midbrain)

Brain lesion in: Mammillary bodies (bilateral)

Consequence: Wernicke-Korsakoff syndrome (confusion, confabulation, ophthalmoplegia, ataxia)

Wernicke-Korsakoff syndrome (confusion, confabulation, ophthalmoplegia, ataxia) Where is the lesion?

Mammillary bodies (bilateral)

Brain lesion in: Basal ganglia

Consequence: May result in tremor at rest, chorea, or athetosis

May result in tremor at rest, chorea, or athetosis Where is the lesion?

Basal ganglia

Brain lesion in: Cerebellar hemisphere

(hint: cerebellar hemispheres are laterally located, so they affect the lateral limbs) Consequence: Intention tremor, limb ataxia; Damage to the cerebellum results in ipsilateral deficits; Fall toward side of lesion

Intention tremor, limb ataxia; Damage to the cerebellum results in ipsilateral deficits; Fall toward side of lesion Where is the lesion?

Cerebellar hemisphere (hint: cerebellar hemispheres are laterally located, so they affect the lateral limbs)

Brain lesion in: Cerebellar vermis

(hint: vermis is centrally located, so it affects the central body) Consequence: Truncal ataxia, dysarthria.

Truncal ataxia, dysarthria. Where is the lesion?

Cerebellar vermis (hint: vermis is centrally located, so it affects the central body)

Brain lesion in: Subthalamic nucleus

Consequence: Contralateral hemiballismus

Contralateral hemiballismus Where is the lesion?

Subthalamic nucleus

Brain lesion in: Hippocampus

Consequence: Anterograde amnesia -- inability to make new memories

Anterograde amnesia -- inability to make new memories Where is the lesion?

Hippocampus

Brain lesion in: Paramedian pontine reticular formation (PPRF)

Consequence: Eyes look away from side of lesion

Eyes look away from side of lesion Where is the lesion?

Paramedian pontine reticular formation (PPRF)

Brain lesion in: Frontal eye fields

Consequence: Eyes look toward lesion.

Eyes look toward lesion. Where is the lesion?

Frontal eye fields

Aphasia (definition) vs. Dysarthria (definition)

Aphasia is a higher-order inability to speak. vs. Dysarthria is a motor inability to speak.

Broca's aphasia

Nonfluent aphasia w/ intact comprehension. Broca's area -- inferior frontal gyrus. ("Bro ca's Bro ken Boca " [boca = mouth in Spanish])

Wernicke's aphasia

Fluent aphasia with impaired comprehension. Wernicke's area -- superior temporal gyrus. ("W ernicke's is W ordy but makes no sense." or "W ernicke's = W hat?")

Global aphasia

Nonfluent aphasia w/ impaired comprehension. Both Broca's and Wernicke's areas affected.

Conduction aphasia

Poor repitition but fluent speech, intact comprehension. Arcuate fasciculus -- connects Broca's and Wernicke's areas.

Anterior cerebral artery: what areas of cortex does it supply?

Supplies anteromedial surface of brain [darkest grey] <img src="400a Cerebral arteries.JPG" />

Middle cerebral artery: what areas of cortex does it supply?

Supplies lateral surface of brain [White areas below] <img src="400a Cerebral arteries.JPG" />

Posterior cerebral artery: what areas of cortex does it supply?

Supplies posterior and inferior surfaces [medium grey areas below] <img src="400a Cerebral arteries.JPG" />

Anterior cerebral artery: Where is it? <img src="401b Circle of Willis without labels.JPG" /> What does it supply?

[Right anterior cerebral artery is labeled below -- top/left] <img src="401a Circle of Willis with labels.JPG" /> Supplies medial surface of the brain, leg-foot area of motor and sensory cortices.

Middle cerebral artery: Where is it? <img src="401b Circle of Willis without labels.JPG" /> What does it supply?

[Labeled below at top/left, just beneath right anterior cerebral art.] <img src="401a Circle of Willis with labels.JPG" /> Supplies lateral aspect of brain, trunk-arm-face area of motor and sensory cortices, Broca's and Wernicke's speech areas (on dominant hemisphere), optic radiations.

What deficit occurs w/ problems in the middle cerebral artery?

Contralateral face and arm paralysis and sensory loss, aphasia (dominant sphere), left-sided neglect.

Posterior cerebral artery: Where is it? <img src="401b Circle of Willis without labels.JPG" /> What does it supply?

[labeled below along middle/right] <img src="401a Circle of Willis with labels.JPG" /> Supplies the visual cortex.

What deficit is associated with problems in the posterior cerebral artery?

Contralateral homonymous hemianopia with macular sparing.

Anterior communicating artery: Where is it? <img src="401b Circle of Willis without labels.JPG" /> What is associated with this artery?

[labeled below along top/right] <img src="401a Circle of Willis with labels.JPG" /> Most common site of circle of Willis aneurysm; lesions may cause visual field defects.

Posterior communicating artery: Where is it? <img src="401b Circle of Willis without labels.JPG" /> What is associated with this artery?

[labeled below along middle/left] <img src="401a Circle of Willis with labels.JPG" /> Common area of aneurysm; Causes CN III palsy.

Lateral striate: Where are they? <img src="401b Circle of Willis without labels.JPG" /> What do they supply?

[labeled below along middle/right] <img src="401a Circle of Willis with labels.JPG" /> Divisions of the middle cerebral artery that supply the internal capsule, caudate, putamen, and globus pallidus.

What deficit is associated with the lateral striate?

"Arteries of stroke"; infarct of internal capsule causes pure motor hemiparesis.

Watershed zones of the circle of Willis

Between anterior cerebral/middle cerebral, posterior cerebral/middle cerebral arteries. Damaged in severe hypotension --< upper leg/upper arm weakness, defects in higher-order visual processing.

Posterior Inferior Cerebellar Artery (PICA): Where is it? <img src="401b Circle of Willis without labels.JPG" /> What deficits are associated with an infarct here?

[labled below at bottom/right] <img src="401a Circle of Willis with labels.JPG" /> Infarcts cause Wallenberg's syndrome (aka lateral medullary syndrome) (nystagmus, ipsilateral ataxia, nausea, vomiting, Horner's syndrome)

Basilar artery: Where is it? <img src="401b Circle of Willis without labels.JPG" /> What would an infarct here cause?

[labeled below along middle/left] <img src="401b Circle of Willis without labels.JPG" /> Infarct causes locked-in syndrome.

In general, strokes of the anterior circle of Willis vs. the posterior circle of Willis

stroke of the anterior circle : General sensory and motor dysfunction, aphasia. stroke of the posterior circle : Cranial nerve deficits (vertigo, visual deficits), coma, cerebellar deficits (ataxia)

Anterior spinal artery: Where is it? <img src="401b Circle of Willis without labels.JPG" /> What defects are associated?

[at bottom of picture, below] <img src="401a Circle of Willis with labels.JPG" /> Medial medullary syndrome: contralateral hemiparesis (lower extremities), medial lemniscus (decr proprioception), ipsilateral paralysis of hypoglossal nerve

Anterior Inferior Cerebellar Artery (AICA) Where is it located? <img src="401b Circle of Willis without labels.JPG" /> What deficits are associated?

[labeled below in lower right] <img src="401a Circle of Willis with labels.JPG" /> Lateral inferior pontine syndrome: ipsilateral facial paralysis, ipsilateral cochlear nucleus, vestibular (nystagmus), ipsilateral facial pain and temperature, ipsilateral dystaxia (MCP, ICP)

Berry aneurysms: Where do they occur? What is the most common complication?

<img src="554a Berry aneurysms.JPG" /> Occur at the bifurcations in the circle of Willis. Most common site is bifurcation of the anterior communicating artery. Rupture (most common complication) leads to hemorrhagic stroke/subarachnoid hemorrhage.

Berry aneurysms: associated with? other risk factors?

Associated with: Adult polycystic kidney dz Ehlers-Danlos syndrome Marfan's syndome Risk factors: Advanced age HTN Smoking Race (higher risk in blacks)

Charcot-Bouchard microaneurysms: Associated with? What do they affect?

Associated with chronic HTN Affects small vessels (e.g., in basal ganglia, thalamus)

Epidural hematoma

<img src="402a epidural hematoma.JPG" /> Rupture of middle meningeal artery (branch of maxillary artery), often secondary to fracture of temporal bone. Lucid interval. CT shows "biconvex disk" not crossing suture lines. Can cross falx, tentorium. <img src="554b Epidural hematoma.JPG" />

Subdural hematoma

<img src="402b subdural hematoma.JPG" /> Rupture of bridging veins. Venous bleeding (less pressure) with delayed onset of Sx's. Seen in elderly individuals, alcoholics, blunt trauma, shaken baby. Crescent-shaped hemorrhage that crosses suture lines. Cannot cross falx, tentorium. <img src="554c Subdural hemorrhage.JPG" />

Factors predisposing to a subdural hematoma

Brain atrophy Shaking Whiplash

Subarachnoid hemorrhage

<img src="402c Subarachnoid hemorrhage.JPG" /> Rupture of aneurysm (usually berry aneurysm) or an AVM. Pts complain of "worst headache of my life." Bloody or yellow (xanthochromic) spinal tap. 2-3 days afterward, there is a risk of vasospasm (Tx w/ Ca2+ channel blockers).

Parenchymal hematoma

Caused by HTN, amyloid angiopathy [see below], DM, and tumor. Typically occurs in basal ganglia and internal capsule. <img src="556a Amyloidosis.JPG" />

Hemorrhagic stroke

Intracerebral bleeding, often due to aneurysm rupture. May be secondary to ischemic stroke following reperfusion (incr vessel fragility)

Ischemic stroke

Emboli block large vessels; etiologies include: atrial fibrillation, carotid dissection, patent foramen ovale, endocarditis. Lacunar strokes block small vessels, are secondary to HTN. Tx: tPA w/in 3 hours.

Transient Ischemic Attack (TIA)

Brief, reversible episode of neurologic dysfunction due to focal ischemia. Typically, Sx's last >24 hours.

Stroke imaging

Bright on diffusion-weighted MRI in 3-30 minutes [below/left], dark on CT in ~24 hours [below/right] <img src="403a Right MCA stroke MRI.JPG" /><img src="403b Right MCA stroke CT.JPG" /> [Images are of a right MCA stroke; diffusion MRI and CT]

Dural venous sinuses: Where do they run? What is the sequence?

Venous sinuses run in the dura mater where its meningeal and periosteal layers separate. Cerebral veins --< venous sinuses --< internal jugular vein <img src="403c Dural venous sinuses with labels.JPG" />

Where is the supereior sagittal sinus? The confluence of the sinuses? The Occipital sinus? The Transverse and sigmoid sinuses? <img src="403d Dural venous sinuses without labels.JPG" />

The superior sagittal sinus (main location of CSF return via arachnoid granulations) is along the superior/median border of the brain. The confluence of the sinuses is posterior, bringing together the occipital sinus (inferiorly), sagittal sinus (superiorly), transverse sinuses (laterally), and straight sinus (ventrally) <img src="403c Dural venous sinuses with labels.JPG" />

Where is the inferior sagittal sinus? The Great cerebral vein (of Galen)? The Straight sinus? <img src="403d Dural venous sinuses without labels.JPG" />

The inferior sagittal sinus runs deep to the superior sagittal sinus in the median line. The great cerebral vein runs inferior to that, and the two sinuses meet at the straight sinus, which feeds into the confluence of the sinuses posteriorly. <img src="403c Dural venous sinuses with labels.JPG" />

What is one vein that feeds into the dural venous sinuses?

The Superior ophthalmic vein feeds into the cavernous sinus, which reaches the sup. sagittal sinus and the transverse sinus by way of the Sphenoparietal sinus. <img src="403c Dural venous sinuses with labels.JPG" />

Where is CSF made? Where is reabsorbed?

CSF is made by ependymal cells lining the ventricles; it is reabsorbed by venous sinus arachnoid granulations.

What connects the lateral to the 3rd ventricle?

The foramen of Munro. <img src="404a Ventricular system.JPG" />

What connects the 3rd and 4th ventricles?

The cerebral aqueduct <img src="404a Ventricular system.JPG" />

What connects the 4th ventricle and the subarachnoid space?

Foramina of L ushka = L ateral Foramen of M agendie = M edial <img src="404a Ventricular system.JPG" />

Hydrocephalus

<img src="404b Hydrocephalus.JPG" /> Accumulation of excess CSF in ventricular system --< increased intracranial pressure; ventricular dilation --< clinical triad of dementia, gait problems, urinary incontenincence. ("Wet, wobbly, and wacky")

Normal pressure (communicating) hydrocephalus

Caused by impaired absorption of CSF by arachnoid granulations (e.g., arachnoid adhesions post-meningitis)

Obstructive (non-communicating) hydrocephalus

Caused by structual blockage of CSF circulation w/in the ventricular system (e.g., stenosis of the aqueduct of Sylvius)

Hydrocephalus ex vacuo

Appearance of increased CSF in atrophy. Intracranial pressure normal, triad not seen.

Total # of spinal nerves? Per section?

There are 31 spinal nerves. ("31 like the 31 flavors at Baskin-Robbins") 8 Cervical 12 Thoracic 5 Lumbar 5 Sacral 1 Coccygeal

Numbering of cervical spinal nerves

Nerves C1-C7 exit via intervertebral foramina above the corresponding vertebra. All other nerves exit below .

Where does vertebral disk herniation usually occur?

Vertebral disk herniation (nucleus pulposus hernaites through annulus fibrosus) usually occurs btw L5 and S1.

How far does the spinal cord extend in adults? The subarachnoid space? Where do you perform a lumbar puncture?

In adults, the spinal cord extends to the loweer border of L1-L2; subarachnoid space extends to lower border of S2. Lumbar puncture is usually performed in L3-L4 or L4-L5 interspaces, at the level of the cauda equina. ("To keep the cord alive , keep the spinal needle btw L3 and L5 ")

Where do you get CSF from in a lumbar puncture?

CSF is obtained from lumbar subarachnoid space btw L4 and L5 (at the level of iliac crests) <img src="405a Lumbar puncture.JPG" />

Structures pierced in a lumbar puncture (in order)

1.) Skin/superficial fascia 2.) Ligaments (supraspinous, interspinous, ligamentum flavum) 3.) Epidural space 4.) Dura mater 5.) Subdural space 6.) Arachnoid 7.) Subarachnoid space - CSF (Pia is not pie rced) <img src="405a Lumbar puncture.JPG" />

What do the dorsal columns of the spinal cord relay?

Pressure, vibration, touch, proprioception. <img src="405b Spinal cord and associated tracts.JPG" />

How are the dorsal columns of the spinal cord organized?

Medially: fasciculus gracilis (lower body, extremities) Laterally: fasciculus cuneatus (upper body, extremities) ("Dorsal column is organized as you are, with hands at sides. Arms outside, legs inside.") <img src="405b Spinal cord and associated tracts.JPG" />

What do the lateral corticospinal tract and spinothalamic tract relay? Where are they located? How are they organized?

Lateral corticospinal tract relays voluntary motor information, is located in the lateral spinal cord. Spinothalamic tract relays pain and temperature, is located antero-laterally. ("L egs are L ateral in L ateral corticospinal, spinothalamic tracts") <img src="405b Spinal cord and associated tracts.JPG" />

What arteries follow the spinal cord?

2 Posterior spinal arteries, 1 anterior spinal artery <img src="405b Spinal cord and associated tracts.JPG" />

Where are the intermediate horn sympathetics found?

The lateral gray matter of the thoracic [only] spinal cord <img src="405b Spinal cord and associated tracts.JPG" />

Ascending spinal tracts and synapsing

They synapse then cross.

Spinal tract: Dorsal column -- medial lemniscal pathway

function? Ascending pressure, vibration, touch, and proprioceptive sensation

Ascending pressure, vibration, touch, and proprioceptive sensation what spinal tract is this?

Dorsal column -- medial lemniscal pathway

Spinal tract: Spinothalamic tract

function? Ascending pain and temperature sensation

Ascending pain and temperature sensation what spinal tract is this?

Spinothalamic tract

Spinal tract: Lateral corticospinal tract

function? Descending vvoluntary movement of contralateral limbs

Descending vvoluntary movement of contralateral limbs what spinal tract is this?

Lateral corticospinal tract

Spinal tract: Dorsal column -- medial lemniscal pathway

What is the 1st order neuron? Sensory nerve ending --< cell body in dorsal root ganglion --< enters spinal cord, ascends ipsilaterally in dorsal column

Sensory nerve ending --< cell body in dorsal root ganglion --< enters spinal cord, ascends ipsilaterally in dorsal column This is the 1st order neuron in which spinal tract?

Dorsal column -- medial lemniscal pathway

Spinal tract: Spinothalamic tract

What is the 1st order neuron? Sensory nerve ending (A-delta and C fibers) (cell body in dorsal root ganglion) --< enters spinal cord

Sensory nerve ending (A-delta and C fibers) (cell body in dorsal root ganglion) --< enters spinal cord This is the 1st order neuron in which spinal tract?

Spinothalamic tract

Spinal tract: Lateral corticospinal tract

What is the 1st order neuron? Upper motor neuron: cell body in primary motor cortex | Descends ipsilaterally (thru internal capsule) until decussating at caudal medulla (pyramidal decussation) | Descends contralaterally

Upper motor neuron: cell body in primary motor cortex | Descends ipsilaterally (thru internal capsule) until decussating at caudal medulla (pyramidal decussation) | Descends contralaterally This is the 1st order neuron in which spinal tract?

Lateral corticospinal tract

Spinal tract: Dorsal column -- medial lemniscal pathway

What is the 1st synapse? Ipsilateral nucleus cuneatus or gracilis (medulla)

Ipsilateral nucleus cuneatus or gracilis (medulla) This is the 1st synapse in which spinal tract?

Dorsal column -- medial lemniscal pathway

Spinal tract: Spinothalamic tract

What is the 1st synapse? Ipsilateral gray matter (spinal cord)

Ipsilateral gray matter (spinal cord) This is the 1st synapse in which spinal tract?

Spinothalamic tract

Spinal tract: Lateral corticospinal tract

What is the 1st synapse? Cell body of anterior horn (spinal cord)

Cell body of anterior horn (spinal cord) This is the 1st synapse in which spinal tract?

Lateral corticospinal tract

Spinal tract: Dorsal column -- medial lemniscal pathway

What is the 2nd order neuron? Decussates in medulla --< ascends contralaterally in medial lemniscus

Decussates in medulla --< ascends contralaterally in medial lemniscus This is the 2nd order neuron in which spinal tract?

Dorsal column -- medial lemniscal pathway

Spinal tract: Spinothalamic tract

What is the 2nd order neuron? Decussates at anterior white commissure --< ascends contralaterally

Decussates at anterior white commissure --< ascends contralaterally This is the 2nd order neuron in which spinal tract?

Spinothalamic tract

Spinal tract: Lateral corticospinal tract

What is the 2nd order neuron? Lower motor neuron : leaves spinal cord

Lower motor neuron : leaves spinal cord This is the 2nd order neuron in which spinal tract?

Lateral corticospinal tract

Spinal tract: Dorsal column -- medial lemniscal pathway OR Spinothalamic tract

What is the 2nd synapse? VPL of thalamus

VPL of thalamus This is the 2nd synapse in which spinal tract?

Dorsal column -- medial lemniscal pathway OR Spinothalamic tract

Spinal tract: Lateral corticospinal tract

What is the 2nd synapse? Neuromuscular junction

Neuromuscular junction This is the 2nd synapse in which spinal tract?

Lateral corticospinal tract

Spinal tract: Dorsal colum -- medial lemniscal pathway OR Spinothalamic tract

What is the 3rd order neuron? Sensory cortex

Sensory cortex This is the 3rd order neuron in which spinal tract?

Dorsal colum -- medial lemniscal pathway OR Spinothalamic tract

Spinal tract: Lateral corticospinal tract

What is the 3rd order neuron? N/A (no 3rd-order neuron)

N/A (no 3rd-order neuron) This is the 3rd order neuron in which spinal tract?

Lateral corticospinal tract

Lower vs. Upper motor neuron lesion

Lower MN lesion = everything lowered (less muscle mass, decr muscle tone, decr reflexes, downgoing toes) Upper MN = everythinig up (tone, DTRs, toes)

Spinal tract: UMN vs. LMN lesion: Weakness

What is the 3rd order neuron? Both

Both

This is the 3rd order neuron in which spinal tract? UMN vs. LMN lesion: Weakness

Spinal tract: UMN vs. LMN lesion: Atrophy

What is the 3rd order neuron? (-) UMN (+) LMN

(-) UMN (+) LMN This is the 3rd order neuron in which spinal tract?

UMN vs. LMN lesion: Atrophy

Spinal tract: UMN vs. LMN lesion: Fasciculations (muscle twitching)

What is the 3rd order neuron? (-) UMN (+) LMN

(-) UMN (+) LMN This is the 3rd order neuron in which spinal tract?

UMN vs. LMN lesion: Fasciculations (muscle twitching)

Spinal tract: UMN vs. LMN lesion: Reflexes

What is the 3rd order neuron? Increased in UMN Decreaseed in LMN

Increased in UMN Decreaseed in LMN This is the 3rd order neuron in which spinal tract?

UMN vs. LMN lesion: Reflexes

Spinal tract: UMN vs. LMN lesion: Tone

What is the 3rd order neuron? Increased in UMN, decreased in LMN

Increased in UMN, decreased in LMN This is the 3rd order neuron in which spinal tract?

UMN vs. LMN lesion: Tone

Spinal tract: UMN vs. LMN lesion: Babinski sign (upgoing toes -- normal in infants)

What is the 3rd order neuron? (+) in UMN, (-) in LMN

(+) in UMN, (-) in LMN This is the 3rd order neuron in which spinal tract?

UMN vs. LMN lesion: Babinski sign (upgoing toes -- normal in infants)

Spinal tract: UMN vs. LMN lesion: Spastic paralysis

What is the 3rd order neuron? (+) in UMN (-) in LMN

(+) in UMN (-) in LMN This is the 3rd order neuron in which spinal tract?

UMN vs. LMN lesion: Spastic paralysis

Spinal cord lesions: Poliomyelitis and Werdnig-Hoffmann disease What areas are affected? What are the Sx?

Lower motor neuron lesion only, due to destruction of anterior horns; flaccid paralysis <img src="407a Polio and WH dz.JPG" />

Lower motor neuron lesion only, due to destruction of anterior horns; flaccid paralysis <img src="407a Polio and WH dz.JPG" /> What spinal cord lesion is this?

Poliomyelitis and Werdnig-Hoffmann disease

Spinal cord lesions: Multiple sclerosis What areas are affected? What are the Sx?

Mostly white matter of cervical region; random and asymmetric lesions, due to demyelination; scanning speech, intention tremor, nystagmus <img src="407b MS.JPG" />

Mostly white matter of cervical region; random and asymmetric lesions, due to demyelination; scanning speech, intention tremor, nystagmus <img src="407b MS.JPG" /> What spinal cord lesion is this?

Multiple sclerosis

Spinal cord lesions: ALS What areas are affected? What are the Sx?

Combined upper and lower motor neuron deficits with no sensory deficit; both upper and lower motor neuron signs. <img src="407c ALS.JPG" />

Combined upper and lower motor neuron deficits with no sensory deficit; both upper and lower motor neuron signs. <img src="407c ALS.JPG" /> What spinal cord lesion is this?

ALS

Spinal cord lesions: Complete occlusion of the anterior spinal artery What areas are affected? What are the Sx?

Spares dorsal columns and tract of Lissauer; upper throacicc ASA territory is a watershed area, as artery of Adamkiewicz supplies ASA below ~T8 <img src="407d Complete occlusion of ASA.JPG" />

Spares dorsal columns and tract of Lissauer; upper throacicc ASA territory is a watershed area, as artery of Adamkiewicz supplies ASA below ~T8 <img src="407d Complete occlusion of ASA.JPG" /> What spinal cord lesion is this?

Complete occlusion of the anterior spinal artery

Spinal cord lesions: Tabes dorsalis (tertiary syphilis) What areas are affected? What are the Sx?

Degeneration of dorsal roots and dorsal columns; impaired proprioception, locomotor ataxia <img src="407e Tabes Dorsalis.JPG" />

Degeneration of dorsal roots and dorsal columns; impaired proprioception, locomotor ataxia <img src="407e Tabes Dorsalis.JPG" /> What spinal cord lesion is this?

Tabes dorsalis (tertiary syphilis)

Spinal cord lesions: Syringomyelia What areas are affected? What are the Sx?

Crossing fibers of spinothalamic tract damaged; bilateral loss of pain and temperature sensation. <img src="407f Syringomyelia.JPG" />

Crossing fibers of spinothalamic tract damaged; bilateral loss of pain and temperature sensation. <img src="407f Syringomyelia.JPG" /> What spinal cord lesion is this?

Syringomyelia

Spinal cord lesions: Vitamin B12 neuropathy and Friedrich's ataxia What areas are affected? What are the Sx?

Demyelination of dorsal columns, lateral corticospinal tracts, and spinocerebellar tracts; ataxic gait, hyperreflexia, impaired position and vibration sense. <img src="407g B12 def and Freidrichs ataxia.JPG" />

Vitamin B12 neuropathy and Friedrich's ataxia

Poliomyelitis: Cause? Transmission? Replication? Pathogenesis?

Caused by poliovirus, which is transmitted by fecal/oral route. Replciates in the oropharynx and small intestine before spreading through the bloodstream to the CNS, where it leads to destruction of cells in the anterior horn of the spinal cord, leading in turn to LMN destruction.

Poliomyelitis: Sx?

Malaise, hedache, fever, nausea, abdominal pain, sore throat. Signs of LMN lesions -- muscle weakness and atrohphy, fasciculations, fibrillation, and hyporeflexia.

Poliomyelitis: Findings?

CSF w/ lymphocytic pleocytosis w/ slight elevation of protein (w/ no change in CSF glucose). Virus recovered from stool or throat.

Werdnig-Hoffman dz (aka infantile spinal muscular atrophy)

Autosomal-recessive inheritance; presents at birth as a "floppy baby," tongue fasciculations; median age of death 7 months. Associated w/ degenration of anterior horns. LMN involvement only.

Amyotrophic lateral sclerosis (commonly known as Lou Gehrig's dz)

Associated w/ both LMN and UMN signs; no sensory, cognitive, or oculomotor deficits. Can be caused by defect in superoxide dismutase 1 (SOD1), betel nut ingestion.

Tabes dorsalis

Degeneration of dorsal columns and dorsal roots due to tertiary syphilis, resulting in impaired proprioception and locomotor ataxia. <img src="408a Tabes dorsalis.JPG" />

Associated with Tabes dorsalis

Charcot's joints Shooting (lightning) pain Argyll Robertson pupils (aka "prostitute's pupils" - accomodate, but do not react) Absence of DTRs <img src="546a Tabes dorsalis.JPG" />

Friedrich's ataxia: Inheritance? Etiology? Sx? Onset?

Autosomal-recessive trinucleotide repeat disorder (GAA; frataxin gene). Leads to impairment in mitochondrial functioning. Staggering gait, frequent falling, nystagmus, dysarthria, hypertrophic cardiomyopathy. Presents in childhood w/ kyphoscoliosis.

Brown-Séquard Syndrome: What is it?

Heisection of the spinal cord <img src="408b B-S syndrome lesion.JPG" />

Brown-Séquard Syndrome: Findings?

1.) Ipsilateral UMN signs (corticospinal tract) below lesion 2.) Ipsilateral loss of tactile, vibration, proprioception sense (dorsal column) below lesion 3.) Contralateral pain and temperature loss (spinothalamic tract) below lesion 4.) Ipsilateral loss of all sensation at level of lesion 5.) LMN signs (e.g., flaccid paralysis) at level of lesion If lesion occurs above T1, presents w/ Horner's syndrome <img src="408c B-S syndrome body map.JPG" />

Horner's syndrome

Sympathectomy of face: 1.) P tosis (slight drooping of eyelid) 2.) A nhidrosis (absence of sweating) and flushing (rubor) of affected side of face 3.) M iosis (pupil constriction) ("PAM is horny [Horner's]) Associated w/ lesion of spinal cord above T1 (e.g., Pancoast's tumor, Brown-Séquard syndrome [cord hemisection], late-stage syringomyelia)

3 Neuron pathway involved in Horner's syndrome

<img src="409a Horners syndrome.JPG" /> The 3-neuron oculosympathetic pathway projects from the hypothalamus to the intermediolateral column of the spinal cord, then to the superior cervical (sympathetic) ganglion, and finally to the pupil, the smooth muscle of the eyelids, and the sweat glands of the forehead and face. Interruption of any of these pathways results in Horner's syndrome.

Clinically important landmarks for a pudendal nerve block (to relieve pain of pregnancy)

Ischial spine

Clinically important landmarks for Appendix

2/3 of the way from the umbilicus to the anterior superior iliac spine (McBurney's point)

Clinically important landmarks for lumbar puncture

Iliac crest.

Landmark dermatomes: C2

Posterior half of a skull "cap" <img src="409b Landmark dermatomes.JPG" />

Landmark dermatomes: C3

High turtleneck shirt <img src="409b Landmark dermatomes.JPG" />

Landmark dermatomes: C4

Low-collar shirt <img src="409b Landmark dermatomes.JPG" />

Landmark dermatomes: T4

At the nipple. (T4 at the teat pore ) <img src="409b Landmark dermatomes.JPG" />

Landmark dermatomes: T7

Xiphoid process <img src="409b Landmark dermatomes.JPG" />

Landmark dermatomes: T10

At the umbilicus (important for early appendicitis pain referral) (T10 at the belly butTEN ) <img src="409b Landmark dermatomes.JPG" />

Landmark dermatomes: L1

At the inguinal ligament ("L1 is IL [I nguinal L igament]) <img src="409b Landmark dermatomes.JPG" />

Landmark dermatomes: L4

Includes kneecaps <img src="409b Landmark dermatomes.JPG" />

Landmark dermatomes: S2, S3, S4

Erection and sensation of penile and anal zones ("S2, 3, 4, keep the penis off the floor") <img src="409b Landmark dermatomes.JPG" />

Muscle spindles vs. Golgi tendon organs

Muscle spindles monitor muscle length (help you pick up a heavy suitcase when you didnt know how heavy it was). Golgi T endon organs monitor muscle T ension (make you drop a heavy suitcase you've been holding too long).

Muscle spindle: pathway?

In parallel with muscle fibers. Muscle stretch --< intrafusal stretch --< stimulates Ia afferent --< stimulate alpha motor neuron --< reflex muscle (extrafusal) contraction <img src="410a Spindle muscle control.JPG" />

Spindle muscle control: the Gamma loop

CNS stimulates gamma motor neuron --< contracts intrafusal fiber --< increased sensitivity of reflex arc <img src="410a Spindle muscle control.JPG" />

Clinical reflexes and their respective nerve roots: Achilles? Patella? Biceps? Triceps?

Achilles = S1 nerve root Patella = L4 nerve root Biceps = C5 nerve root Triceps = C7 nerve root <img src="410b Clinical reflexes.JPG" /> * Note that they count up in order: S1,2 L3,4 C5,6 C7,8

Babinski sign

Dorsiflexion of the big toe and fanning of other toes; sign of UMN lesion, but normal reflex in 1st year of life.

Primitive reflexes

Normally disappear within 1st year of life. May reemerge following frontal lobe lesion. Include: Moro reflex, rooting reflex, suckling reflex, Palmar and plantar reflexes, Babinski reflex

Moro reflex

Extension of limbs when started

Rooting reflex

Movement of head toward one side if cheek or mouth is stroked (nipple seeking)

Sucking reflex

Sucking response when roof of mouth is touched

Palmar and palantar reflexes

Curling of fingers/toes if palms of hands/feet are stroked

Cranial nerves that lie medially at the brainstem

III, VI, XII Remember: 3 (x2) = 6 (x2) = 12

Brain stem: could you label these structures? <img src="411b Brain stem without labels.JPG" />

Which cranial nerve arises dorsally and emerges ventrally?

CN IV [see below, CN IV is along left in the middle] <img src="411a Brain stem with labels.JPG" />

Dorsal brainstem structures: Pineal gland

Melatonin secretion, circadian rhythms. <img src="411c Dorsal brainstem.JPG" />

Dorsal brainstem structures: superior colliculi

Conjugate vertical gaze center. ("you have your eyes above your ears, and the superior colliculus (visual) is above the inferior colliculus (auditory).") <img src="411c Dorsal brainstem.JPG" />

Dorsal brainstem structures: inferior colliculi

Auditory ("you have your eyes above your ears, and the superior colliculus (visual) is above the inferior colliculus (auditory).") <img src="411c Dorsal brainstem.JPG" />

Parinaud syndrome

Paralysis of conjugate verticle gaze due to lesion in superior colliculi (e.g., pinealoma)

Cranial nerves: Olfactory (CN I) function? type? mnemonic?

Smell (only CN w/o thalamic relay to cortex) S ensory; "S ome" [Mnemonic for type of information carried by CN's: "Some Say Marry Money, But My Brother Says Big Brains Matter Most."]

Which cranial nerve is this? (Function, type, mnemonic) Smell (only CN w/o thalamic relay to cortex) S ensory; "S ome" [Mnemonic for type of information carried by CN's: "Some Say Marry Money, But My Brother Says Big Brains Matter Most."]

Olfactory (CN I)

Cranial nerves: Optic (CN II) function? type? mnemonic?

Sight. S ensory; "S ay" [Mnemonic for type of information carried by CN's: "Some Say Marry Money, But My Brother Says Big Brains Matter Most."]

Which cranial nerve is this? (Function, type, mnemonic) Sight. S ensory; "S ay" [Mnemonic for type of information carried by CN's: "Some Say Marry Money, But My Brother Says Big Brains Matter Most."]

Optic (CN II)

Cranial nerves: Oculomotor (CN III) function? type? mnemonic?

Eye movement (SR, IR, MR, IO), pupillary constriction, accommodation, eyelid opening (levator palpebrae) M otor; "M oney" [Mnemonic for type of information carried by CN's: "Some Say Marry Money, But My Brother Says Big Brains Matter Most."]

Which cranial nerve is this? (Function, type, mnemonic) Eye movement (SR, IR, MR, IO), pupillary constriction, accommodation, eyelid opening (levator palpebrae) M otor; "M oney" [Mnemonic for type of information carried by CN's: "Some Say Marry Money, But My Brother Says Big Brains Matter Most."]

Oculomotor (CN III)

Cranial nerves: Trochlear (CN IV) function? type? mnemonic?

Eye movement (SO) M otor; "M oney" [Mnemonic for type of information carried by CN's: "Some Say Marry Money, But My Brother Says Big Brains Matter Most."]

Which cranial nerve is this? (Function, type, mnemonic) Eye movement (SO) M otor; "M oney" [Mnemonic for type of information carried by CN's: "Some Say Marry Money, But My Brother Says Big Brains Matter Most."]

Trochlear (CN IV)

Cranial nerves: Trigeminal (CN V) function? type? mnemonic?

Mastication, facial sensation. B oth, "B ut" [Mnemonic for type of information carried by CN's: "Some Say Marry Money, But My Brother Says Big Brains Matter Most."]

Which cranial nerve is this? (Function, type, mnemonic) Mastication, facial sensation.

B oth, "B ut" [Mnemonic for type of information carried by CN's: "Some Say Marry Money, But My Brother Says Big Brains Matter Most."] Trigeminal (CN V)

Cranial nerves: Abducens (CN VI) function? type? mnemonic?

Eye movement (LR) M otor; "M y" [Mnemonic for type of information carried by CN's: "Some Say Marry Money, But My Brother Says Big Brains Matter Most."]

Which cranial nerve is this? (Function, type, mnemonic) Eye movement (LR) M otor; "M y" [Mnemonic for type of information carried by CN's: "Some Say Marry Money, But My Brother Says Big Brains Matter Most."]

Abducens (CN VI)

Cranial nerves: Facial (CN VII) function? type? mnemonic?

Facial movement, taste from anterior 2/3rds of tongue, lacrimation, salivation (submandibular and sublingual glands), eyelid closing (orbicularis oculi), stapedius muscle in ear B oth; "B rother" [Mnemonic for type of information carried by CN's: "Some Say Marry Money, But My Brother Says Big Brains Matter Most."]

Which cranial nerve is this? (Function, type, mnemonic) Facial movement, taste from anterior 2/3rds of tongue, lacrimation, salivation (submandibular and sublingual glands), eyelid closing (orbicularis oculi), stapedius muscle in ear B oth; "B rother" [Mnemonic for type of information carried by CN's: "Some Say Marry Money, But My Brother Says Big Brains Matter Most."]

Facial (CN VII)

Cranial nerves: Vestibulocochlear (CN VIII) function? type? mnemonic?

Hearing, balance. S ensory; "S ays" [Mnemonic for type of information carried by CN's: "Some Say Marry Money, But My Brother Says Big Brains Matter Most."]

Which cranial nerve is this? (Function, type, mnemonic) Hearing, balance. S ensory; "S ays" [Mnemonic for type of information carried by CN's: "Some Say Marry Money, But My Brother Says Big Brains Matter Most."]

Vestibulocochlear (CN VIII)

Cranial nerves: Glossopharyngeal (CN IX) function? type? mnemonic?

Taste from posterior 1/3rd of tongue, swallowing, salivation (parotid gland), monitoring carotid body and sinus chemo- and baroreceptors, and stylopharyngeus (elevates pharynx, larynx) B oth; "B ig" [Mnemonic for type of information carried by CN's: "Some Say Marry Money, But My Brother Says Big Brains Matter Most."]

Which cranial nerve is this? (Function, type, mnemonic) Taste from posterior 1/3rd of tongue, swallowing, salivation (parotid gland), monitoring carotid body and sinus chemo- and baroreceptors, and stylopharyngeus (elevates pharynx, larynx) B oth; "B ig" [Mnemonic for type of information carried by CN's: "Some Say Marry Money, But My Brother Says Big Brains Matter Most."]

Glossopharyngeal (CN IX)

Cranial nerves: Vagus (CN X) function? type? mnemonic?

Taste from epiglottic region, swallowing, palate elevation, talking, coughing, thoracoabdominal viscera, monitoring aortic arch chemo- and baroreceptors. B oth; "B rains" [Mnemonic for type of information carried by CN's: "Some Say Marry Money, But My Brother Says Big Brains Matter Most."]

Which cranial nerve is this? (Function, type, mnemonic) Taste from epiglottic region, swallowing, palate elevation, talking, coughing, thoracoabdominal viscera, monitoring aortic arch chemo- and baroreceptors. B oth; "B rains" [Mnemonic for type of information carried by CN's: "Some Say Marry Money, But My Brother Says Big Brains Matter Most."]

Vagus (CN X)

Cranial nerves: Accessory (CN XI) function? type? mnemonic?

Head turning, shoulder shrugging M otor; "M atter" [Mnemonic for type of information carried by CN's: "Some Say Marry Money, But My Brother Says Big Brains Matter Most."]

Which cranial nerve is this? (Function, type, mnemonic) Head turning, shoulder shrugging M otor; "M atter" [Mnemonic for type of information carried by CN's: "Some Say Marry Money, But My Brother Says Big Brains Matter Most."]

Accessory (CN XI)

Cranial nerves: Hypoglossal (CN XII) function? type? mnemonic?

Tongue movement M otor; "M ore" [Mnemonic for type of information carried by CN's: "Some Say Marry Money, But My Brother Says Big Brains Matter Most."]

Which cranial nerve is this? (Function, type, mnemonic) Tongue movement M otor; "M ore" [Mnemonic for type of information carried by CN's: "Some Say Marry Money, But My Brother Says Big Brains Matter Most."]

Hypoglossal (CN XII)

Cranial nerve nuclei: Where are they located, generally?

Located in tegmentum portion of brainstem (btw dorsal and ventral portions). Lateral nuclei = sensory M edial nuclei = M otor

Cranial nerve nuclei located in the midbrain

Nuclei of CN III and IV

Cranial nerve nuclei located in the pons

Nuclei of CN V, VI, VII, and VIII

Cranial nerve nuclei located in the medulla

Nuclei of CN IX, X, XI, and XII

CN reflexes: Corneal OR Lacrimation (use the same nerves) Afferent? Efferent?

Afferent = V-1 Efferent = VII

Afferent = V-1 Efferent = VII What CN reflex is this?

Corneal OR Lacrimation (use the same nerves)

CN reflexes: Jaw jerk Afferent? Efferent?

Afferent = V-3 (sensory) Efferent = V-3 (motor)

Afferent = V-3 (sensory) Efferent = V-3 (motor) What CN reflex is this?

Jaw jerk

CN reflexes: Pupillary Afferent? Efferent?

Afferent = II Efferent = III

Afferent = II Efferent = III What CN reflex is this?

Pupillary

CN reflexes: Gag Afferent? Efferent?

Afferent = IX Efferent = IX and X

Afferent = IX Efferent = IX and X What CN reflex is this?

Gag

Vagal nuclei: Nucleus Solitarious

Visceral S ensory information (e.g., taste, baroreceptors, gut distension) CN VII, IX, X ("S olitarius = viS ceral S ensory")

Vagal nuclei: Nucleus ambiguous

M otor innervation of pharynx, larynx, and upper esophagus (e.g., swallowing, palate elevation) CN's IX, X, XI ("aM biguous = M otor")

Vagal nuclei: Dorsal motor nucleus

Sends autonomic (parasympathetic) fibers to heart, lungs, and upper GI.

Cranial nerve and vessel pathways: What exits via the cribiform plate?

CN I

Cranial nerve and vessel pathways: What exits via the middle cranial fossa?

CN II-VI, thru the sphenoid bone: 1.) Optic canal : CN II, ophthalmic artery, central retinal vein 2.) S uperior orbital fissure : CN III, IV, V-1, VI, ophthalmic vein 3.) Foramen R otundum : CN V-2 4.) Foramen O vale : CN V-3 5.) Foramen spinosum : middle meningeal artery ("Divisions of CN-V exit owing to S tanding R oom O nly")

Cranial nerve and vessel pathways: What exits via the Posterior cranial fossa?

CN VII-XII, thru the temporal and occipital bone: 1.) Internal auditory meatus : CN VII, VIII 2.) Jugular foramen : CN IX, X, XI, jugular vein 3.) Hypoglossal canal : CN XII 4.) Foramen magnum : Spinal roots of CN XI, brain stem, vertebral arteries

What/where is the cavernous sinus? What is the route of blood thru it?

A collection of venous sinuses on either side of the pituitary. Blood from eye and superficial cortex | Cavernous sinus | Internal jugular vein <img src="414a Cavernous sinus.JPG" />

What nerves pass through the cavernous sinus?

CN II, IV, V-1, V-2, VI, and postganglionic sympathetic fibers en route to the orbit all pass thru the cavernous sinus. Only CN VI is "free-floating". Cavernous portion of internal carotid artery is also here.

What is cavernous sinus syndrome?

Nerves that control extraocular muscles (plus V-1 and V-2) pass thru the cavernous sinus. Therefore, cavernous sinus syndrome (e.g., due to mass effect): ophthalmoplegia, ophthalmic and maxillary sensory loss. <img src="414a Cavernous sinus.JPG" />

CN XII lesion (LMN) What is the defect?

Tongue deviates toward the side of the lesion ("lick your wounds")

CN V motor lesion What is the defect?

Jaw deviates toward the side of lesion

CN X lesion what is the defect?

Uvula deviates away from side of lesion

CN XI lesion what is the defect?

Weakness turning head to contralateral side of lesion. Shoulder droop on side of lesion.

Facial lesions: UMN lesion

Lesion of motor cortex or connection btw cortex and facial nucleus. Contralateral paralysis of lower face only, since upper face recives bilateral UMN innervation. <img src="415a Facial lesions.JPG" />

Facial lesions: LMN lesion

Ipsilateral paralysis of upper and lower face. <img src="415a Facial lesions.JPG" />

Facial lesions: Bell's palsy

Complete destruction of the facial nucleus itself or its branchial efferent fibers (facial nerve proper) Peripheral ipsilateral facial paralysis w/ inability to close eye on involved side. Can occur idiopathically; gradual recovery in most cases. <img src="415a Facial lesions.JPG" />

In what dz's/disorders is Bell's palsy seen as a complication?

A IDS L yme dz H erpes zoster S arcoidosis T umors D iabetes ("AL exander graH am Bell with STD ")

KLM sounds (kuh, la, mi)

Say it aloud. "Kuh-kuh-kuh" tests palate elevation (CN X - vagus) "La-la-la" tests tongue (CN XII - hypoglossal) "Mi-mi-mi" tests lips (CN VII - facial) ("It would be a K aL aM ity to lose CN X, XII, and VII")

Muscles of mastication

3 Muscles close jaw: M asseter, teM poralis, and M edial pterygoid ("M 's M unch") 1 Muscle opens jaw: Lateral pterygoid ("Lateral Lowers" -- [lateral pterygoid]) All above are innervated by the trigeminal nerve (V-3)

Muscles with glossus

All muscles with the root glossus in their names (except palatoglossus, innervated by vagus nerve) are innervated by the hypoglossal nerve. Palat : vagus nerve Glossus : hypoglossal nerve

Muscles with palat

All muscles with the root palat in their names (except tensor veli palatini , innervated by mandibular branch of CN V) are innervated by vagus nerve. Palat : vagus nerve (except TENS or, who was too TENSE )

Inner ear as a "series of tubes"

A series of tubes in the temporal bone (bony labrynth) filled with perilymph (Na+ rich, similar to ECF) that includes cochlea, vestibule, and semicircular canals. W/in the bony labyrinth is a 2nd series of tubes (membranous labyrinth) filled w/ endolymph (K+ risch, similar to ICF) that includes cochlear duct (w/in the cochlea), utricle and saccule (w/in the vestibule), and semicircular canals. *peri = think outside of the cell (Na+), vs. Endo = think inside the cell (K+) <img src="416a Inner ear.JPG" />

Where is the endolymph (of the inner ear) made?

Made by the stria vascularis.

What do the utricle and saccule contain? What do they detect?

Contain maculae - detect linear acceleration.

What do the semicircular canals contain? What do they detect?

Contain A mpullae, detect A ngular acceleration.

Hair cells (of the inner ear): Where are they? What do they do?

Located w/in the organ of Corti. Are the sensory elements in both vestibular apparatus (spatial orientation) and cochlea (hearing).

How can you remember where frequencies are sensed along the cochlear membrane?

The cochlear membrane = scuba flipper: narrow/stiff at the base (high frequency), and wide/flexible at the apex (low frequency). <img src="416b cochlear membrane.JPG" />

Conductive hearing loss

Bone conduction < air conduction on Rinne; Weber localizes to the affected ear.

Sensorineural hearing loss

Air conduction < Bone conduction on Rinne; Weber localizes to normal ear.

Hearing loss in the elderly

High frequency --< low frequency

Could you label this picture? <img src="417b Eye and retina without labels.JPG" />

Answers <img src="417a Eye and retina without labels.JPG" />

What are the muscles that make up the iris? What receptors do they have, and what are their effects?

Dilator/radial muscle (alpha1 --< myd riasis [pupillary d ilation]) Sphincter/circular/constrictor muscle (M3 --< miosis [pupillary constriction]) <img src="417c Aqueous humor pathway.JPG" />

Where are the ciliary muscles? What receptors do they have, and what effect?

Shown below/right. M3 --< accomodation <img src="417c Aqueous humor pathway.JPG" />

Where is aqueous humor made? Where is it reabsorbed? [give the whole pathway]

Aqueous humor is made by ciliary process | Travels past lens to posterior Chamber | Anterior chamber | Trabecular meshwork (absorbs aqueous humor | Canal of Schlemm (collects aqueous humor from trabecular meshwork) <img src="417c Aqueous humor pathway.JPG" />

Glaucoma (general pathogenesis)

Impaired flow of aqueous humor | Increased intraocular pressure | Optic disk atrophy w/ cupping

Open angle glaucoma

Obstructed outflow (e.g., canal of Schlemm); associated w/ myopia, advanced age, African-American race. More common, "silent," painless.

Closed angle glaucoma

Obstruction of flow btw iris, lens --< pressure builds up behind iris. Painful, impaired vision. Do NOT give epinephrine.

Cataract

Painless, bilateral opacification of lens, leading to decrease in vision. Risk factors: age, smoking, EtOH, sunlight, DM, trauma, infxn.

Papilledema

Increased intracranial pressure --< elevated optic disk with blurred margins, bigger blind spot.

Innervation of the extraocular muscles?

CN VI innervates the L ateral R ectus CN IV innervates the S uperior O blique CN III innervates the R est Thus, the "chemical formula": LR6 SO4 R3 <img src="418c Extraocular eye muscles and nerves.JPG" />

What are the 3 actions of the superior oblique?

It abducts, intorts, and depresses.

CN III damage

Eye looks down and out; ptosis, pupillary dilation, loss of accomodation.

CN IV damage

Diplopia w/ defective downward gaze

CN VI damage

Medially directed eye.

Testing extraocular muscles

To test fxn of each muscle, have te pt look in the following directions: <img src="419a testing intraocular muscles.JPG" /> [*note that the oblique muscles are tested by looking medially and opposite to what you would expect from "superior" and "inferior"] "IOU : to test I nferior O blique, have pt look U p."

Strabismus vs. Amblyopia

Strabismus is misalignment of eyes. Multiple etiologies. Amblyopia is a reduction of vision from disuse in critical period. May be secondary to strabismus, deprivation, unequal refractive errors.

What controls pupillary constriction (miosis)

P upillary sphincter muscle, P arasympathetic innervation. Innervation -- CN III from Edinger-Westphal nucleus --< ciliary ganglion.

What controls pupillary D ilation (myD riasis)?

RaD ial muscle (aka pupillary D ilator muscle), sympathetic. Innervation -- T1 preganglionic sympathetic --< superior cervical ganglion --< postganglionic sympathetic --< long ciliary nerve.

Pupillary light reflex

Light in either retina sends a signal via CN II to pretectal nuclei (dashed lines, below) in midbrain that activate bilateral Edinger-Westphal nuclei; pupils constrict bilaterally (consensual reflex). Result: illumination of 1 eye results in bilateral pupillary constriction. <img src="419b Pupillary light reflex.JPG" />

Marcus Gunn pupil

Afferent pupillary defect (e.g., due to optic nerve damage or retinal detachment). Decreased bilateral pupillary constriction when light is shone in affected eye. <img src="419b Pupillary light reflex.JPG" />

CN III in cross-section

Center carries output to ocular muscles, affected primarily by vascular disease (e.g., DM) Outside carries parasympathetic output, affected 1st by compression (e.g., PCA berry aneurysm, uncal herniation); use pupillary light reflex in assessment, "blown pupil" <img src="420a CNIII in cross-section.JPG" />

Retinal detachment

Separation of neurosensory layer of retina from pigment epithelium | Degeneration of photoreceptors | Vision loss May be secondary to trauma, diabetes.

Age-related macular degeneration (ARMD)

Degeneration of macula (central area of retina). Causes loss of central vision (scotomas). "Dry"/atrophic ARMD is slow, causes gradual decrease in vision "Wet" ARMD is rapid, due to neovascularization.

Visual field defects: Right anopia What would this look like in the visual field? Where is the lesion?

#1, below <img src="420b Visual field defects.JPG" />

#1, below <img src="420b Visual field defects.JPG" /> What is this visual field defect called?

Right anopia

Visual field defects: Bitemporal hemianopia What would this look like in the visual field? Where is the lesion?

#2, below <img src="420b Visual field defects.JPG" />

#2, below <img src="420b Visual field defects.JPG" /> What is this visual field defect called?

Bitemporal hemianopia

Visual field defects: Left homonymous hemianopia What would this look like in the visual field? Where is the lesion?

#3, below <img src="420b Visual field defects.JPG" />

#3, below <img src="420b Visual field defects.JPG" /> What is this visual field defect called?

Left homonymous hemianopia

Visual field defects: Left upper quadrantic anopia (right temporal lesion) What would this look like in the visual field? Where is the lesion?

#4, below <img src="420b Visual field defects.JPG" />

#4, below <img src="420b Visual field defects.JPG" /> What is this visual field defect called?

Left upper quadrantic anopia (right temporal lesion)

Visual field defects: Left lower quadrantic anopia (right parietal lesion) What would this look like in the visual field? Where is the lesion?

#5, below <img src="420b Visual field defects.JPG" />

#5, below <img src="420b Visual field defects.JPG" /> What is this visual field defect called?

Left lower quadrantic anopia (right parietal lesion)

Visual field defects: Left hemianopia w/ macular sparing What would this look like in the visual field? Where is the lesion?

#6, below <img src="420b Visual field defects.JPG" />

#6, below <img src="420b Visual field defects.JPG" /> What is this visual field defect called?

Left hemianopia w/ macular sparing

Visual field defects: Central scotoma (macular degeneration) What would this look like in the visual field? Where is the lesion?

#7, below <img src="420b Visual field defects.JPG" />

#7, below <img src="420b Visual field defects.JPG" /> What is this visual field defect called?

Central scotoma (macular degeneration)

Internuclear ophthalmoplegia (MLF syndrome)

Lesion in the medial longitudinal fasciculus (MLF) --< medial rectus palsy on attempted lateral gaze. Nystagmus in abducting eye. Convergence normal. Syndrome is seen in many pts w/ multiple sclerosis ("M LF = M S") <img src="421a Internuclear opthalmoplegia.JPG" /> When looking left, the left nucleus of CN VI fires, which contracts the lateral rectus and stimulates the contralateral (right) nucleus of CN III via the right MLF to contract the right medial rectus. <img src="421b Looking L with R MLF damage.JPG" />

Dementia (defined)

Decreased cognitive ability, memory, fxn, with intact consciousness.

Alzheimer's dz: Epidemiology? Groups at increased risk?

Most common cause of dementia in the elderly. Down syndrome pts are at increased risk of developing AD.

Alzheimer's dz: genetics?

Familial form (10%) assocaited w/ genes on chromosomes 1, 14, 19 (APOE4 allele; autosomal dominant), and 21 (p-App ) gene.

Alzheimer's dz: pathogenesis?

Widespread, accelerated cortical atrophy with decreased ACh. <img src="553a Alzheimers Dz.JPG" /> Associated w/ senile plaques (extracellular, beta-amyloid core) and neurofibrillary tangles (intracellular, abnormally phosphorylated tau protein; tangles correlate w/ degree of dementia). May cause amyloid angiopathy --< intracranial hemorrhage.

Pick's dz (frontotemporal dementia)

Dementia, aphasia, parkinsonian aspects; Associated w/ Pick bodies (intracellular, aggregated tau protein), frontotemporal lobe atrophy. Spares parietal lobe and posterior 2/3rds of superior temporal gyrus.

Lewy body dementia

Parkinsonism with dementia and hallucinations. Caused by alpha-synuclein defect.

Creutzfeldt-Jakob dz (CJD)

Rapidly progressive (wks-mos) dementia w/ myoclonus, spongiform cortex; associated w/ prions.

"Other" causes of dementia

Multi-infarct (2nd most common cause of dementia in the elderly) Syphilis HIV Vitamin B12 deficiency Wilson's dz

Multiple sclerosis: What is it?

Autoimmune inflammation and demyelination of CNS (brain and spinal cord).

Multiple sclerosis: How do pts present? What is the course of the dz?

Pts can present with: optic neuritis (sudden loss of vision) MLF syndrome (internuclear ophthalmoplegia) Hemiparesis Hemisensory Sx's Bowel/bladder incontinence. Relapsing and remitting course.

Multiple sclerosis: Who is affected?

Most often affects women in their 20s and 30s; more common in whites.

Findings in multiple sclerosis

Elevated protein (IgG) in CSF. Periventricular plaques (areas of oligodendrocyte loss and reactive gliosis) w/ preservation of axons. <img src="555b MS.JPG" />

Charcot's triad of MS

Charcot's traid of MS is a SIN : S canning speech I ntention tremor (+I ncontinence, I nternuclear ophthalmoplegia) N ystagmus

Tx for multiple sclerosis

Beta-interferon or immunosuppressant therapy. Symptomatic Tx for neurogenic bladder, spasticity, and pain.

Guillan-Barre syndrome (acute inflammatory demyelinating polyradiculopathy) What is it/what are the main Sx?

Inflammation and demyelination of peripheral nerves and motor fibers of ventral roots (sensory effect less severe than motor), causing symmetric ascending muscle weakness beginning in distal lower extremities. Facial paralysis in 50% of cases. Autonomic fxn may be severely affected (e.g., cardiac irregularities, HTN, or hypotension).

Guillan-Barre syndrome (acute inflammatory demyelinating polyradiculopathy) What is the prognosis?

Almost all pts survive; the majority recover completely after wks to months.

Guillan-Barre syndrome (acute inflammatory demyelinating polyradiculopathy): Findings?

Elevated CSF protein w/ normal cell count (albuminocytologic dissociation). Elevated protein --< papilledema.

Guillan-Barre syndrome (acute inflammatory demyelinating polyradiculopathy): is associated with...?

Associated with infxns --< autoimmune attack of peripheral myelin due to molecular mimicry (e.g., Campylobacter jejuni or herpesvirus infxn), inoculations, and stress, but no definitive link to pathogens.

Guillan-Barre syndrome (acute inflammatory demyelinating polyradiculopathy): Management/Tx?

Respiratory support is critical until recovery. Additional Tx: plasmapheresis, IV immune globulins.

Progressive multifocal leukoencephalopathy (PML)

Demyelination of CNS due to destruction of oligodendrocytes. Associated w/ JC virus and seen in 2-4% of AIDS pts (reactivation of latent viral infxn). Rapidly progressive, usually fatal.

Acute disseminated (postinfectious) encephalomyelitis

Multifocal perivenular inflammation and demyelination after infxn (e.g., chickenpox, measles) or certain vaccinations (e.g., rabies, smallpox)

Metachromatic leukodystrophy

Autosomal-recessive lysosomal storage dz, most commonly due to arylsulfatase A deficiency. Builup of sulfatides leads to impaired production of myelin sheath.

Charcot-Marie Tooth disease (aka hereditary motor and sensory neuropathy HMSN)

Group of progressive hereditary nerve d/o's related to defective production of proteins involved in the structure and fxn onf peripheral nerves or the myelin sheath.

Seizure

Characterized by synchronized, high-frequency neuronal firing. Variety of forms.

Partial seizures

1 area of brain. Most commonly originates in the mesial temporal lobe. Often preceded by seizure aura; can secondarily generalize.

2 types of partial seizures

1.) Simple partial (consciousness intact): motor, sensory, autonomic, psychic 2.) Complex partial (impaired consciousness)

Generalized seizures

Diffuse.

5 Types of generalized seizures

1.) Absence (petit mal) - blank stare 2.) Myoclonic - quick, repetitive jerks 3.) Tonic-clonic (grand mal) - alternating stiffening and movement 4.) Tonic - stiffening 5.) Atonic - "drop" seizures (falls to floor); commonly mistaken for fainting

Epilepsy

A d/o of recurrent seizures (febrile seizures are not epilsepsy)

Causes of seizures by age: Children?

Genetic Infxn (febrile) Trauma Congenital Metabolic

Causes of seizures by age: Adults?

Tumors Trauma Stroke Infxn

Causes of seizures by age: Elderly?

Stroke Tumor Trauma Metabolic Infxn

Headache (definition)

Pain due to irritation of structures such as dura, cranial nerves, or extracranial structures, not brain parenchyma itself.

Migrain headache

4-72 hours of unilateral pulsating pain w/ nausea, photophobia, or phonophobia. +/- "aura" of neurologic Sx before HA, including visual dsensory, speech disturbances. Due to irritation of CN V and release of substance P, CGRP, vasoactive peptides.

Tension headache

< 30 minutes of bilateral steady pain. Not aggravated by light or noise; no aura.

Cluster headache

Repetitive brief headaches characterized by unilateral periorbital pain associated w/ ipsilateral lacrimation, rhinorrhea, Horner's syndrome. Much more common in males.

"Other" causes of headache

Subarachnoid hemorrhage ("worst headache of my life") Meningitis Hydrocephalus Neoplasia Arteritis

Vertigo (definition)

Illusion of movement, not to be confused w/ dizziness or lightheadedness.

Peripheral vertigo

More common type. Inner ear etiology (e.g., semicircular canal debris, vestibular nerve infxn, Meniere's dz). Positional testing --< delayed horizontal nystagmus.

Central vertigo

Brain stem or cerebellar lesion (e.g., vestibular nuclei, posterior fossa tumor). Positional testing --< immediate nystagmus in any direction; may change directions.

Neurocutaneous disorders: Sturge-Weber syndrome

Congenital d/o w/ port-wine stains and ipsilateral leptomeningeal angioma. Can cause glaucoma, seizures, hemiparesis, and mental retardation. Occurs sporadically.

Neurocutaneous disorders: Tuberous sclerosis

Hamartomas in CNS, skin, organs; cardiac rhabdomyoma, renal agiomyolipoma, subependymal giant cell astrocytoma, MR, seizures, hypopigmented "ash leaf spots," sebaceous adenoma, shagreen patch. Autosomal dominant.

Neurocutaneous disorders: Neurofibromatosis type I (von Recklinghausen's disease)

Café-au-lait spots Lisch nodules (pigmented iris hamartomas) Neurofibromas in skin. Autosomal dominant

Neurocutaneous disorders: von Hippel-Lindau dz

Cavernous hemangiomas in skin, mucosa, organs; renal cell carcinoma hemangioblastoa in retina, brain stem, cerebellum. Autosomal dominant.

Primary brain tumors

Clinical presentation due to mass effects (e.g., seizures, demential, focal lesions); Primary tumors rarely undergo metastasis. The majority of adult primary tumors are supratentorial, while the majority of childhood primary tumors are infratentorial. Note: half of adult brain tumors are metastases (well circumscribed; usually present at the gray-white junction).

Adult peak incidence tumors: Glioblastoma multiforme (grade IV astrocytoma) <img src="425a Supratentorial tumors.JPG" />

Most common primary brain tumor. Prognosis grave; > 1yr life expectancy. Found in cerebral hemispheres. Can cross corpus callosum ("butterfly glioma" [below]) Stain astrocytes for GFAP. <img src="555c Glioblastoma.JPG" /> "Pseudopalisading" pleomorphic tumor cells -- border central areas of necrosis and hemorrhage [above/right]

Glioblastoma multiforme (grade IV astrocytoma) <img src="425a Supratentorial tumors.JPG" />

Adult peak incidence tumors: Meningioma <img src="425a Supratentorial tumors.JPG" />

2nd most common primary brain tumor. Most often occurs in convexities of hemispheres and parasagittal region. Arises from arachnoid cells external to brain. Resectable. Spindle cells concentrically arranged in a whorled pattern; psammoma bodies (laminated calcifications).

Meningioma <img src="425a Supratentorial tumors.JPG" />

Adult peak incidence tumors: Schwannoma <img src="425b Infratentorial tumors.JPG" />

3rd most common primary brain tumor. Schwann cell origin; often localized to CN VIII --< acoustic schwannoma. Resectable. Bilateral schwannoma found in neurofibromatosis type II.

Adult peak incidence tumors: Oligodendroma <img src="425a Supratentorial tumors.JPG" />

Relatively rare, slow groing. Most often in frontal lobes. Chicken-wire capillary pattern. <img src="555d oligodendroglioma.JPG" />' Oligodendrocytes = "fried egg" cells -- round nuclei w/ clear cytoplasm. Often calcified in oligodendroglioma.

Adult peak incidence tumors: Pituitary adenoma <img src="425a Supratentorial tumors.JPG" />

Most commonly prolactinoma. Bitemporal hemianopia (due to pressure on optic chiasm) and hyper- or hypopituitarism are sequelae. Rathke's pouch.

Childhood peak incidence tumors: Pilocytic (low-grade) astocytoma <img src="425b Infratentorial tumors.JPG" />

Usually well circumscribed. In children, most often found in posterior fossa. May be supratentorial. GFAP positive. Benign; good prognosis. Rosenthal fibers -- eosinophilic, corkscrew fibers.

Usually well circumscribed. In children, most often found in posterior fossa. May be supratentorial. GFAP positive. Benign; good prognosis. Rosenthal fibers -- eosinophilic, corkscrew fibers. What tumor does this describe?

Pilocytic (low-grade) astocytoma <img src="425b Infratentorial tumors.JPG" />

Childhood peak incidence tumors: Medullo-blastoma <img src="425b Infratentorial tumors.JPG" />

Highly malignant cerebellar tumor. A form of primitive neuroectodermal tumor (PNET). Can compress 4th ventricle, causing hydrocephalus. Rosettes or perivascular pseudorosette pattern cells. Radiosensitive.

Medullo-blastoma <img src="425b Infratentorial tumors.JPG" />

Childhood peak incidence tumors: Ependymoma <img src="425b Infratentorial tumors.JPG" />

Ependymal cell tumors most commonly found in 4th ventricle. Can cause hydrocephalus. Poor prognosis. Characteristic perivascular pseudorosettes. Rod-shaped blepharoplasts (basal ciliary bodies) found near nucleus.

Ependymoma <img src="425b Infratentorial tumors.JPG" />

Childhood peak incidence tumors: Hemangioblastoma <img src="425b Infratentorial tumors.JPG" />

Most often cerebellar; associated w/ von Hippel-Lindau syndrome when found w/ retinal angiomas. Can produce EPO --< secondary polycythemia. Foamy cells and high vascularity are characteristic.

Most often cerebellar; associated w/ von Hippel-Lindau syndrome when found w/ retinal angiomas. Can produce EPO --< secondary polycythemia. Foamy cells and high vascularity are characteristic. What tumor does this describe?

Hemangioblastoma <img src="425b Infratentorial tumors.JPG" />

Childhood peak incidence tumors: Craniopharyngioma <img src="425b Infratentorial tumors.JPG" />

Benign childood tumor, confused w/ pituitary adenoma (can also cause bitemporal hemianopia). Most common childhood supratentorial tumor. Derived from remnants of Rathke's pouch. Calcification is common (tooth enamel-like).

Craniopharyngioma <img src="425b Infratentorial tumors.JPG" />

Herniation syndromes: Cingulate (subfalcine) herniation under falx cerebri

Can compress anterior cerebral artery. #1 below: <img src="426a Herniation syndromes.JPG" />

Can compress anterior cerebral artery. #1 below: <img src="426a Herniation syndromes.JPG" /> What herniation syndrome is this?

Cingulate (subfalcine) herniation under falx cerebri

Herniation syndromes: Downward transtentorial (central) herniation

#2 below <img src="426a Herniation syndromes.JPG" />

#2 below <img src="426a Herniation syndromes.JPG" /> What herniation syndrome is this?

Downward transtentorial (central) herniation

Herniation syndromes: Uncal herniation

(hint: Uncus = medial temporal lobe) #3 below: <img src="426a Herniation syndromes.JPG" />

#3 below: <img src="426a Herniation syndromes.JPG" /> What herniation syndrome is this?

Uncal herniation (hint: Uncus = medial temporal lobe)

Herniation syndromes: Cerebellar tonsillar herniation into the foramen magnum

#4 below: <img src="426a Herniation syndromes.JPG" />

#4 below: <img src="426a Herniation syndromes.JPG" /> What herniation syndrome is this?

Cerebellar tonsillar herniation into the foramen magnum

Hernation syndromes: what is the biggest danger?

Coma and death result when these hernations compress the brain stem.

Clinical signs of uncal herniation: Ipsilateral dilated pupil/pstosis

Stretching of CN III (innervates levator palpebrae)

Clinical signs of uncal herniation: Contralateral homonymous hemianopia

Compression of ipsilateral posterior cerebral artery

Clinical signs of uncal herniation: Ipsilateral paresis

Compression of contralateral crus cerebri (Kernohan's notch)

Clinical signs of uncal herniation: Duret hemorrhages -- paramedian artery rupture

Caudal displacement of brain stem.

Epinephrine Class of drug? Mechanism? SE's?

alpha-agonist. Decreases aqueous humor synthesis due to vasoconstriction. SE: mydriasis, stinging; do not use in closed-angle glaucoma.

Brimonide Class of drug? Mechanism? SE's?

alpha-agonist. Decreased aqueous humor synthesis. SE: no pupillary or vision changes.

Timolol, betaxolol, carteolol Class of drug? Mechanism? SE's?

beta-blockers. Decrease aqueous humor secretion SE: no pupillary or vision changes.

Acetazolamide Class of drug? Mechanism? SE's?

Diuretic. Decrease aqueous humor secretion due to decreased HCO3- (via inhibition of carbonic anhydrase) SE: no pupillary or vision changes.

Pilocarpine, carbachol, physostigmine, echothiophate Class of drug? Mechanism? SE's?

Cholinomimetics Increase outflow of aqueous humor; contract ciliary muscle and open trabecular meshwork; use pilocarpine in emergencies; very effective at opening canal of Schlemm. SE: Miosis, cyclospasm.

Latanoprost (PGF-2alpha) Class of drug? Mechanism? SE's?

Prostaglandin. Increases outflow of aqueous humor. SE: darkens color of iris (browning).

Opioid analgesics (list)

Morphine Fentanyl Codeine Heroin Methadone Meperidine Dextromethorphan

Mechanism of opioid analgesics

Act as agonists at opioid receptors (mu = morphine, delta = enkephalin, kappa = dynorphin) to modulate synaptic transmission -- open K+ channels, close Ca2+ channels, leading to decrease in synaptic transmission.

Clinical toxicity of opioid analgesics

Pain cough suppression (dextromethorphan) diarrhea (loperamide and diphenoxylate) acute pulmonary edema maintenance programs for addicts (methadone)

Toxicity of opioid analgesics

Addiction Respiratory depression Constipation Miosis (pinpoint pupils ) Additive CNS depression with other drugs. Tolerance does not develop to miosis and constipation. Toxicity treated w/ naloxone or naltrexone (opioid receptor antagonist).

Mechanism of butorphanol

Partial agonist at opioid mu receptors, agonst at kappa receptors.

Clinical use of butorphanol

Pain; causes less respiratory depression than full agonists.

Toxicity of butorphanol

Causes withdrawal if on full agonist.

Mechanism of tramadol

Very weak opioid agonist; also inhibits serotonin and NE reuptake (works on multiple neurotransmitters -- "tram it all " in).

Clinical use of tramadol

Chronic pain.

Toxicity of tramadol

Similar to opioids. Decreases seizure threshold.

Epilepsy drugs: Phenytoin Use in partial seizures (simple/complex)? Use in generalized seizures (Tonic-clonic/absence/status)? Mechanism? Notes?

Used in partial seizures (simple and complex). 1st line drug for Tonic-clonic seizures. 1st line drug for prophylaxis of status seizures. Mechanism: increased Na+ channel inactivation.

Used in partial seizures (simple and complex). 1st line drug for Tonic-clonic seizures. 1st line drug for prophylaxis of status seizures. Mechanism: increased Na+ channel inactivation. What epilepsy drug does this describe?

Phenytoin

Epilepsy drugs: Carbamezepine Use in partial seizures (simple/complex)? Use in generalized seizures (Tonic-clonic/absence/status)? Mechanism? Notes?

Used for partial seizures (simple and complex). 1st line drug for tonic-clonic seizures. Mechanism: increases Na+ channel inactivation. *Also 1st line drug for trigemnial neuralgia.

Used for partial seizures (simple and complex). 1st line drug for tonic-clonic seizures. Mechanism: increases Na+ channel inactivation. *Also 1st line drug for trigemnial neuralgia. What epilepsy drug does this describe?

Carbamezepine

Epilepsy drugs: Lamotrigine Use in partial seizures (simple/complex)? Use in generalized seizures (Tonic-clonic/absence/status)? Mechanism? Notes?

Used for partial seizures (simple and complex). May be used for tonic-clonic seizures. Mechanism: blocks VG-Na+ channels.

Used for partial seizures (simple and complex). May be used for tonic-clonic seizures. Mechanism: blocks VG-Na+ channels. What epilepsy drug does this describe?

Lamotrigine

Epilepsy drugs: Gabapentin Use in partial seizures (simple/complex)? Use in generalized seizures (Tonic-clonic/absence/status)? Mechanism? Notes?

Used for partial seizures (simple and complex). May be used for tonic-clonic seizures. Mechanism: increases GABA release. *Also used for peripheral neuropathy.

Used for partial seizures (simple and complex). May be used for tonic-clonic seizures. Mechanism: increases GABA release. *Also used for peripheral neuropathy. What epilepsy drug does this describe?

Gabapentin

Epilepsy drugs: Topiramate Use in partial seizures (simple/complex)? Use in generalized seizures (Tonic-clonic/absence/status)? Mechanism? Notes?

Used for partial seizures (simple and complex). May be used for tonic-clonic seizures. Mechanism: blocks Na+ channels, increases GABA action

Used for partial seizures (simple and complex). May be used for tonic-clonic seizures. Mechanism: blocks Na+ channels, increases GABA action What epilepsy drug does this describe?

Topiramate

Epilepsy drugs: Phenobarbital Use in partial seizures (simple/complex)? Use in generalized seizures (Tonic-clonic/absence/status)? Mechanism? Notes?

Used for partial seizures (simple and complex). May be used for tonic-clonic seizures. Mechanism: increases GABA-A action. *1st line in pregnant women, children.

Used for partial seizures (simple and complex). May be used for tonic-clonic seizures. Mechanism: increases GABA-A action. *1st line in pregnant women, children. What epilepsy drug does this describe?

Phenobarbital

Epilepsy drugs: Valproic acid Use in partial seizures (simple/complex)? Use in generalized seizures (Tonic-clonic/absence/status)? Mechanism? Notes?

Used for partial seizures (simple and complex). 1st line drug for tonic-clonic seizures. May also be used in absence seizures. Mechanism: increases Na+ channel inactivation, increases GABA concentration. *Also used for myoclonic seizures.

Valproic acid

Epilepsy drugs: Ethosuximide Use in partial seizures (simple/complex)? Use in generalized seizures (Tonic-clonic/absence/status)? Mechanism? Notes?

1st line drug for absence seizures. Mechanism: blocks thalamic T-type Ca2+ channels.

1st line drug for absence seizures. Mechanism: blocks thalamic T-type Ca2+ channels. What epilepsy drug does this describe?

Ethosuximide

Epilepsy drugs: Benzodiazepines (diazepam or lorazepam) Use in partial seizures (simple/complex)? Use in generalized seizures (Tonic-clonic/absence/status)? Mechanism? Notes?

1st line for acute status seizures. Mechanism: increase GABA-A action. *Also used for seizures of eclampsia (1st line to prevent seizures of eclampsi is MgSO4)

1st line for acute status seizures. Mechanism: increase GABA-A action. *Also used for seizures of eclampsia (1st line to prevent seizures of eclampsi is MgSO4) What epilepsy drug does this describe?

Benzodiazepines (diazepam or lorazepam)

toxicity of epilepsy drugs: Toxicity of Benzodiazepines

Sedation Tolerance Dependence

toxicity of epilepsy drugs: Toxicity of Carbamazepine

Diplopia Ataxia Blood dyscrasias (agranulocytosis, aplastic anemia) Liver toxicity Teratogenesis Induction of cytochrome P-450

toxicity of epilepsy drugs: Toxicity of ethosuximide

GI distress Fatigue Headache Urticaria Stevens-Johnson syndrome ("EFGH = E thosuximide, F atigue, G I, H eadache")

toxicity of epilepsy drugs: Stevens-Johnson syndrome

prodrome of malaise and fever followed by rapid onset of erythematous/purpuric macules (oral, ocular, genital). Skin lesions progress to epidermal necrosis and sloughing.

toxicity of epilepsy drugs: Toxicity of phenobarbital

Sedation Tolerance Dependence Induction of cytochrome P-450

toxicity of epilepsy drugs: Toxicity of phenytoin

Nystagmus Diplopia Ataxia Sedation Gingival hypreplasia Hirsutism Megaloblastic anemia Teratogenesis SLE-like syndrome Induction of cytochrome P-450

toxicity of epilepsy drugs: Toxicity of valproic acid

GI distress rare but fatal hepatotoxicity (measure LFTs) Neural tube defects in fetus (spina bifida) Tremor Weight gain. Contraindicated in pregnancy.

toxicity of epilepsy drugs: Toxicity of lamotrigine

Stevens-Johnson syndrome

toxicity of epilepsy drugs: Toxicity of Gabapentin

Sedation Ataxia

toxicity of epilepsy drugs: Toxicity of Topiramate

Sedation Mental dulling Kidney stones Weight loss

Mechanism of phenytoin

Use-dependent blockade of Na+ channels; inhibition of glutamate release from excitatory presynaptic neuron.

Clinical use of phenytoin

Tonic-clonic seizures. Also a class IB antiarrhythmic.

Toxicity of phenytoin

Nystagmus, ataxia, diplopia, sedation, SLE-like syndrome, induction of cytochrome P-450. Chronic use produces gingival hyperplasia in children, peripheral neuropathy, hirsutism, megaloblastic anemia (decreased folate absorption). Teratogenic (fetal hydantoin syndrome).

Mechanism of barbiturates (phenobarbital, pentobarbital, thiopental, secobarbital)

Facilitate GABA-A action by increasing duration of Cl- channel opening, thus decreasing neuron firing. ("BarbiDURAT e [increased DURAT ion]")

Clinical use of barbiturates (phenobarbital, pentobarbital, thiopental, secobarbital)

Sedative for anxiety, seizures, insomnia, induction of anestheisa (thiopental)

Toxicity of of barbiturates (phenobarbital, pentobarbital, thiopental, secobarbital)

Dependence, additive CNS depression effects w/ EtOH, respiratory or CV depression (can lead to death), drug interactions owing to induction of liver microsomal enzymes (cytochrome P-450). Tx overdose w/ Sx managment (assist respiration, increase BP) Contraindicated in pregnancy.

Mechanism of benzodiazepines (diazepam, lorazepam, triazolam, temazepam, oxazepam, midazolam, chlordiazepoxide, alprazolam)

Facilitate GABA-A action by increasing frequency of Cl- channel opening. Decreases REM sleep. Most have long half-lives and active metabolites. ("FRE enzodiazepines [increased FRE quency]")

Short acting benzodiazepines

TOM thumb T riazolam O xazepam M idazolam. Highest addictive potential.

Clinical use of benzodiazepines (diazepam, lorazepam, triazolam, temazepam, oxazepam, midazolam, chlordiazepoxide, alprazolam)

Anxiety, spasticity, status epilepticus (lorazepam and diazepam), detoxification (especially EtOH withdrawal - DTs), night terrors, sleep walking.

Toxicity of benzodiazepines (diazepam, lorazepam, triazolam, temazepam, oxazepam, midazolam, chlordiazepoxide, alprazolam)

Dependence, additive CNS depression effects w/ EtOH. Less risk of respiratory depression and coma than w/ barbiturates. Tx overdose w/ flumazenil (competitive antagonist at GABA receptor)

General principles of anesthetics: CNS drugs must be...?

CNS drugs must be lipid soluble (cross the BBB) or be actively transported.

General principles of anesthetics: Solubility and drug effect?

Drugs with low solubility in blood = rapid induction and recovery times. Drugs with high solubility in lipids = high potency = 1 / MAC (where MAC = Minimum Alveolar Concentration at which 50% of the population is anesthetized. Decreases w/ age). e.g., N2O has low blood and lipid solubility, and thus fast induction and low potency. Halothane, in contrast, has high lipid and blood solubility, and thus high potency and slow induction.

Inhaled anesthetics (list)

Halothane Enflurane Isoflurane Sevoflurane Methoxyflurane Nitrous oxide

Mechanism of inhaled anesthetics

Unknown!

Effects of inhaled anesthetics

Myocardial depression Respiratory depression Nausea/emesis Increased cerebral blood flow (decreased cerebral metabolic demand)

Toxicity of inhaled anesthetics

Hepatoxicity (halothane) Nephrotoxicity (methoxyflurane) Proconvulsant (enflurane) Malignant hyperthermia (rare) Expansion of trapped gas (nitrous oxide)

IV anesthetics (list)

B arbiturates B enzodiazepines Arylcyclohexylamins (K etamine) Opiates Propofol ("BB K ing on OPIATES POPO ses FOOL ishly")

Barbiturates (as IV anesthetics)

Thiopental -- high potency, high lipid solubility, rapid entry into brain. Used for induction of anesthesia and short surgical procedures. Effect terminated by redistribution from brain. Decreased cerebral blood flow.

Benzodiazepines (as IV anesthetics)

Midazolam most common drug used for endoscopy; used adjuctively w/ gaseous anesthetics and narcotics. May cause severe postoperative respiratory depression, decr BP (Tx overdose w/ flumazenil), and amnesia.

Arylcyclohexamines (Ketamine) -- as IV anesthetics

PCP analogs that act as dissociative anesthetics. Block NMDA receptors. Cardiovascular stimulants. Cause disorientation, hallucination, and bad dreams. Increase cerebral blood flow.

Opiates (as IV anesthetics)

Morphine, fentanyl used w/ other CNS depressants during general anesthesia.

Propofol (as an IV anesthetic)

Used for rapid anesthesia induction and short procedures. Less postoperative nausea than thiopental. Potentiates GABA-A.

Local anesthetics (list)

Esters Procaine, cocaine, tetracain Amides lI docaI ne, mepI vacaI ne, bupI vacaI ne ("amI des have 2 I 's in their names)

Mechanism of local anesthetics

Block Na+ channels by binding to specific receptors on inner portion of channel. Preferentially bind to activated Na+ channels, so most effecctive in rapidly firing neurons. Tertiary amine local anesthetics penetrate membrane in uncharged form, then bind to ion channels in charged form.

3 principles of local anesthetics

1.) In infected (acidic) tissue, alkaline anesthetics are charged and cannot penetrate membrane effectively. More anesthetic is needed in these cases. 2.) Order of nerve blockade: Small-diameter fibers < large diameter. Myelinated fibers < unmyelinated fibers. Overall, size factor predominates over myelination such that: small myelinated fibers < small unmyelinated fibers < large myelinated fibers < large unmyelinated fibers. Order of loss: pain (lose first) < temperature < touch < pressure (lost last). 3.) Except for cocain, given w/ vasoconstrictors (usually epinephrine) to enhance local action: decreased bleeding, increased anesthesia by decreasing systemic concentration.

Clinical use of local anesthetics

Minor surgical procedures, spinal anesthesia. If allergic to esters, give amides.

Toxicity of local anesthetics

CNS excitation, severe cardiovascular toxicity (bupivacaine), HTN, hypotension, and arrhytmias (cocaine)

Neuromuscular blocking drugs (generally)

Used for muscle paralysis in surgery or mechanical ventilation. Selective for motor (vs. autonomic) nicotinic receptor.

Depolarizing neuromuscular blocking drugs

Succinylcholine (complications include hypercalcemia and hyperkalemia) Reversal of blockade: Phase I (prolonged depolarization) -- no antidote. Block potentiated by cholinesterase inhibitors. Phase II (repolarized but blocked) -- antidote consists of cholinesterase inhibitors (e.g., neostigmine)

Nondepolarizing neuromuscular blocking drugs

Tubocurarine, atracurium, mivacurium, pancuronium, vecuronium, rocuronium. Competitive: compete w/ ACh for receptors. Reversal of blockade: neostigmine, edrophonium, and other cholinesterase inhibitors.

Uses of dantrolene

Used in Tx of malignant hyperthermia, which is caused by the concomitant use of inhalation anesthetics (except N2O) and succinylcholine. Also used to Tx neuroleptic malignant syndrome (a toxicity of antipsychotic drugs)

Mechanism of dantrolene

Prevents the release of Ca2+ from the sarcoplasmic reticulum of skeletal muscle.

What is Parkinson's dz due to (that is addressed by anti-PD drugs)? What agents are used?

Parkinsonism is due to loss of dopaminergic neurons and excess cholinergic activity. "BALSA" B romocriptine A mantadine L evodopa (with carbidopa) S elegiline (and COMT inhibitors) A ntimuscarinics

Parkinson's dz drugs, strategy: Agonize dopamine receptors Agents?

Bromocriptine (ergot alkaloid and partial dopamine agonist) Pramipexole Ropinirole

Parkinson's dz drugs, strategy: Increase dopamine Agents?

Amantadine (may increase dopamine release); also used as an antiviral against influenza A and rubella; toxicity = ataxia. L-dopa/carbidopa (converted to dopamine in the CNS)

Parkinson's dz drugs, strategy: Prevent dopamine breakdown Agents?

Selegiline (selective MAO type B inhibitor); Entacapone, Tolcapone (COMT inhibitors)

Parkinson's dz drugs, strategy: Curb excess cholinergic activity Agents?

Benz tropine (A ntimuscarinic; improves tremor and rigidity but has little effect on bradykinesia). ("Tx your tremor before you drive your Mercedes-BENZ ")

For Tx of essential familly tremors?

Use beta-blocker.

Mechanism of L-dopa (levodopa)/carbidopa

Increase level of dopamine in brain. Unlinke dopamine, L-dopa can cross BBB and is converted by dop decarboxylase in the CNS to dopamine.

Clinical use of L-dopa (levodopa)/carbidopa

Parkinsonism

Toxicity of L-dopa (levodopa)/carbidopa

Arrhythmias from peripheral conversion to dopamine. Long-term use can --< dyskinesia following administration, akinesia btw doses. Carbidopa, a peripheral decarboxylase inhibitor, is given w/ L-dopa in order to increase the bioavailability of L-dopa in the brain and to limit peripheral SE's.

Mechanism of selegiline

Selectively inhibits MAO-B, thereby increasing the availability of dopamine.

Clinical use of selegiline

Adjunctive agent to L-dopa in Tx of Parkinson's dz.

Toxicity of selegiline

May enhance adverse effects of L-dopa.

Mechanism of Sumatriptan

5-HT[1B/1D] agonist. Causes vasoconstriction, inhibition of trigeminal activation and vasoactive peptide release. Half-life is > 2 hours. [the "1B/1D" in brackets is subscript]

Clinical use of sumatriptan

Acute migraine, cluster HA attacks.

Toxicity of Sumatriptan

Coronary vasospasm (contraindicated in pts w/ CAD or Prinzmetal's angina) Mild tingling.

Alzheimer's drugs: Memantine mechanism?

NMDA receptor antagonist; helps prevent excitotoxicity (mediated by Ca2+)

Alzheimer's drugs: Memantine Toxicity?

Dizziness, confusion, hallucinations.

Alzheimer's drugs: Donepezil mechanism?

Acetylcholinesterrase inhibitor

Alzheimer's drugs: Donepezil Toxicity?

Nausea, dizziness, insomnia.

Spina Bifida Occulta Findings

No Herniatn, Intact dura, Hair tuft, Normal AFP

Thalamus Input locations

VPLN - Spinothalamic and dorsal colomns (Pain & Temp)
VPMN - Trigeminal nerve (Taste)
LGN - Optic Nerve (vision)
MGN - Sup. Olive & Inf Coliculi of Tectum (Hearing)
VLN - BG & Cerebellum (motor fx)

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