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256 terms

First Aid Neurology

What originates from the neuroectoderm?
CNS Neurons, Ependymal Cells (inner lining of ventricles, makes CSF), oligodendroglia, astrocytes
What originates from the neural crest cells?
Schwann Cells and PNS Neurons
What originates from the mesoderm?
Microglia, like Macrophages
What are neurons? What is the Nissl substance and where is it located?
Large cells with prominent nucleoli that comprise the nervous system. Nissl Substance (RER) in cell body, dendrites, not axon.
What are some of their functions of astrocytes? What is the astrocyte marker?
Physical Support, Repair, K+ metaboism, removal of excess neurotransmitter, maintenance of blood brain barrier. Reactive gliosis in response to injury,.

Marker is GFAP.
What are the microglia? Origin? Discernible in nissl stains? Morphology

What happens to these guys during tissue damage?

What happens when infected in HIV in the CNS?
CNS Phagocytes. Mesodermal origin. Not readily discernible in the nissl stains. Small irregular nuclei and relatively little cytoplasm.

Tissue damage causes them to turn into large ameboid phagocytic cells.

HIV-infected microglia fuse to form multinucleated giant cells in the CNS.
What is the role of the oligodendroglia? Morphology in Nissl Stains?
Morphology in H and E Stains?

What happens to these cells in MS.
Myelinates multiple CNS axons (up to 30 each).

Small nuclei with dark chromatin and litle type of cytoplasm. Predominant type of glial cell in white matter.

Look like fried eggs in H and E stains.

These cells are destroyed in MS.
What is the role of schwann cells? Where are they derived from?
What happens to these guys in Guillan Barre? Acoustic Neuroma?
Myelinates only 1 PNS axon. Promotes axonal regeneration

Cells destroyed in Guillan Barre Syndrome

Acousitc Neuroma- Type of schwannoma. Typically located in internal acoustic meatus (CN VIII)
What are the types of free nerve endings? Where are they located and what do they sense?
C- slow, unmyelinated fibers
Adelta- fast, myelinated fibers

Located in the skin, epidermis, some viscera

Pain and Temperature
What are meissner's corpuscles? Location? Senses? Adapts quickly or slowly?
Large myelinated fibers located on glabrous (hairless skin). Senses position sense, dynamic fine touch (manipulation). Adapty quickly.
What are paciniam corpuscles? Located?: Senses?
Large, myelinated fibers, deep skin layers, ligaments, and joints. Senses vibration and pressure.
What are Merkel's disks? Located? Senses?
Large myelinated fibers, hair follicles, Position sense, static touch (shapes, edges, textures), adapts slowly
What are the peripheral nerve layers
Endoneurium, Perineurium, and Epineurium
Endoneurium? What will you see in endoneurium in GuillainBarre
Invests single nerve fibers. Inflammatory infiltrate in Guillain Barre.
Perineurium? Surgical clinical correlate?
Surrounds a fascicle of nerve fibers. Must be rejoined in microsurgery for limb reattachment
Dense connective tissue that surrounds entire nerve including fascicles and blood vessels.
Where is NE formed? Changes in what diseases?
Formed in Locus Ceruleus. Increased in anxiety, Decreased in depression.
Where is dopamine formed? Changes in what diseases?
Ventral Tegmentum and Substantia nigra. Increased in schizophrenia, Decreased in depression
Where is serotonin formed? Changes in what diseases?
Raphe Nucleus. Decrease in anxiety and depression
Where is Ach formed? Changes in what diseases?
Basal nucleus of Meynert. Decreased in alzheimers, huntingtons, REM sleep
Where is GABA formed? Changes in what diseases?
Nucleus Accumbens. Decreased in anxiety and huntingtons.
What is Locus Ceruleus for?
Stress and Panic?
What is nucleus accumbens and Septal Nucleus Used for?
Reward Center, pleasure, addiction, fear
What is the Blood Brain Barrier Formed by?
Formed by 3 structures
1. Tight Junctions between nonfenestrated capillary endothelial cells
2. Basement membrane
3. Astrocyte Processes.
What substances cross slowly through blood brain barrier? Rapidly? By what mechanisms
Glucose and amino acids cross slowly by carier mediated transport mechanisms.

Nonpolar/lipid-soluble substances cross rapidly by diffusion.
What happens to areas in the brain with fenestrated capillaries and no blood brain barrier?Give examples
Allow molecules in the blood to affect brain function.
Area postrema- vomiting after chemo, OVLT- osmotic sensing

Neurosecretory products to enter circulation such as ADH from the Neurohypophysis.
What are other examples of barriers?
Blood-Testis Barrier. Maternal-Fetal Blood Barrier of Placenta.
What happens if blood brain barier gets infarcted?
Infarction destroted endothelial cell tight junctions causing vasogenic edema.
What are the functions of the hypothalamus?

What are the inputs to hypothalamus.
Thirst and Water Balance, Adenohypophysis control, Neurohypophsis release hormones from hypothalamus, Hunger, Autonomic Regulation, Temperature regulation, Sexual Urges.

OVLT: senses changes in osmolarity
Area Postrema: Responds to Emetics
What does the supraoptic nucleus make?
What does the Paraventricular nucleus make?
What is the role of the anterior hypothalamus?
Cooling, pArasympathetic
What is the role of the posterior hypothalamus?
Heating and Sympathetics
What is the septal Nucleus responsible for?
Sexual Urges
What is suprachiasmatic nucleus responsible for?
How does leptin affect different areas of the hypothalamus. What are the roles of these different areas of hte hypothalamus? What happens if these are destroyted.
Leptin Inhibits the Lateral Area and Activated the Ventromedial Area.

Lateral Area- responsible for hunger. Destruction results in anorexia, failure to thrive (infants)

Ventromedial Area- Satiety. Destruction (Craniopharyngioma)-> Hyperphagia.
What is the posterior pituitary role?
Receives hypothalamic axonal projections from supraoptic nuclei (ADH) and paraventricular (oxytocin) nuclei.
What is the role of the thalamus?
Major Relay for ascending sensory information that ultimately reaches the cortex.
What is the Lateral Geniculate Nucleus responsible for? Projects via?
Optic Radiations to Occipital Cortex
What is the Medial Geniculate Nucleus Responsible for?
What is the ventral posterior nucleus, lateral part responsible for?
Body sensation (proprioception, pressure, pain, touch, vibration via dorsal columns, spinothalamic tract)
What is the ventral posterior nucleus, medial part responsible for? Via what cranial nerve?
Facial sensation via CNV
What is the ventral anterior/ lateral nuclei responsible for?
What is the blood supply of the thalamus?
Posterior communicating, posterior cerebral, and ICA (Anterior Choroidal Arteries)
What is the limbic system responsible for? What does it consist of?
Feeding, Fleeing, Fighting, Feeling, and Sex.

Consists of cingulate gyrus, hippocampus, fornix, and mamillary bodies.
Function of the Cerebellum? Input? Output?
Receives contralateral cortical input via middle cerebellar peduncle and ipsilateral proprioceptive information via inferior cerebellar peduncle.

Input via the climbing and mossy fibers.

Provides stimulatory feedback to contralateral cortex to modulate movement. Output is via the purkinje fibers to the Deep nuclei of cerebellum, which in turn output to cortex via Superior cerebellar peduncle
What are the Deep Nuclei of the Cerebellum?

Lateral Cerebellum responsible for?
Medial Cerebellum responsible for?
From Lateral to Medial, Dentate, Emboliform, Green, Fastigial

Lateral responsible for voluntary movement of extremities.

Medial responsible for balance, truncal coordination, ataxia, propensity to fall toward injured ipsilateral side

See 395 of first aid for figure.
What is the basal ganglia's role?
Important in voluntary movements and making postural adjustments. Receives cortical inputs and provides negative feedback to cortex to modulate movement.
What is the excitatory pathway of the basal ganglia
SNc dopamine binds to D1 receptors in excitatory pathway, stimulating the excitatroy pathway Loss of dopamine in Parkinson's inhibits the excitatory pathway (Decreases motion).

D1 from SNC stimulates-> Striatrum (Caudate- Cognitive/ Putamen- Motor inhibits)-> GPi/SNr (via GABA/Substance P) which inhibits Thalamus which activates cortex.
What is the Inhibitory Pathway of the Basal Ganglia?
SNc'S dopamine binds to D2 receptors in the inhibitory pathway, inhibiting the inhibitory pathway (increases motion). Loss of dopamine in Parkinson's disinhibits the inhibitory pathway.

D2 from SNC inactivates Striatum which inactivates Gpe (via GABA and Enkephalin) which inactivates STN which activates GpI which inactivates Thalamus which activates Cortex
What happens in Parkinsons? Rare cases seen in?
Degenerative disorder of CNS associated with Lewy bodies (composed of A-synuclein-intracellular inclusion) and depigmentation of substantia nigra pars compacts (loss of dopaminergic neurons.

Rare cases have been linked to exposure to MTPT, a contaminant of illicet street drugs,

Tremor, Cogwheel Rigidity, Akinesia, postural instability
What happens in hemiballismus? What could cause it?
Suden, wild flailing of arm +/- leg
Contralateral subthalamic nucleus lesion (lacunar stroke in a patient with a history of hypertension). Loss of inhibition of thalamus through globus pallidus.
What happens in Huntington's Disease? What will happen to the brain? Mode of inheritance? What chromosome?
Autosomal dominant trinucleotide repeat disorder. Chromosome 4. Neuronal death via NMDA-R binding and glutamate toxicity. Loss in caudate, ACH, and GABA.

Chorea, depression, progressive dementia. Atrophy of Caudate nucleus (loss of GABA), enlarged ventricles, atrophy of putamen, and defined sulci.

Symptoms manifest in affected individuals between 20-50.
Sudden jerky purposeless movements. Characteristics of basal ganglia lesion (Huntington's Disease)
Slow, writhing movements, especially of fingers. Characteristic of basal ganglia lesion (Huntington's)
Sudden, brief muscle contraction. Jerks, hiccups.
Sustained, involuntary muscle contractions. (Writer's Cramps)
Draw a picture of a brain and label where the following would be: Premotor area, Principal Motor Area, Principal Sensory Area, Frontal Eye Fields, Motor Speech (Broca's Area- Dominant Hemisphere), Sylvian Fissure, Arcuate Faciculus, Associative Auditory Cortex (Wernicke's Area Dominant Hemisphere), Primary Auditory Cortex, Primary Visual COrtex, Central Sulcus, Frontal, Parietal, ,Occipital, Temporal Lobe
What are the functions of the frontal lobe?
Executive Funciton- planning, inhibition, concentration, orientation, language, abstraction, judgment, motor regulation, mood,

Lack of social judgement is most notable in frontal lobe lesion. Damage= Disinhibition
What is the homunculus?
Topographical representation of sensory and motor areas in the cerebral cortex. Used to localize lesions (in blood supply) leading to specific deficits.

Lower extremity deficity-> ACA
Damage to amygdala results in what syndrome?
Kluver-Bucy (Hyperorality, Hypersexuality, Disinhibited Behavior)
Frontal Lobe Lesion
Disinhibition and deficits in concentration, orientation, and judgement. Reemergence of primitive reflexes
Right Parietal Lobe Lesion
Spatial Neglect syndrome (Agnosia of contralateral side of the world)
Reticular Activating System Lesion
Reduced Levels of arousal and wakefulness (coma)
Mammillary bodies (Bilateral) lesion
Wernicke Korsakoff Syndrome (Wernicke- Confusion, Opthalmoplegia, ataxia), Korsakoff- memory loss, confabulation, personality changes,
Basal ganglia lesions
Resting Tremor, Chorea, Athetosis
Cerebellar Hemisphere Lesion. Which side do you fall down on and why?
Intention tremor, Limb ataxia, damage to cerebellum results in ipsilateral deficits. Fall toward side of lesion. (Cerebellum-> SCP-> Contralateral Cortex-> corticospinal decussation= ipsilateral)
Cerebellar Vermis lesion
Truncal Ataxia, Dysarthria
Subthalamic Nucleus Lesion
Contralateral Hemiballismus
Hippocampus Lesion
Anterograpde Amensia- inability to make new memories
Paramedian Pontine Reticular Formation Lesion
Eyes look away from side of lesion.
Frontal Eye Fields Lesion
Eyes look Toward Lesion
Recurrent Laryngeal Nerve Injury
Loss of all laryngeal muscles except cricothyroid. Causes hoarseness.
What happens in Central pontine myelinolysis. Caused by?
Acute paralysis, dysarthria, dysphagia, diplopia, loss of consciousness,

Caused by rapid correction of hyponatremia.
What is aphasia?
Higher order inability to speak
What is dysarthria?
Motor inability to speak
What happens in Broca's Aphasia? Where is Broca's area located?
Nonfluent aphasia with intact comprehension. Broca's area- inferior frontal gyrus
What happens in Wernicke's Aphasia?
Where is Wernicke's area located?
Fluent aphasia with impaired comprehension. Wernicke's area- superior temporal gyrus
What happens in global aphasia? What areas affected?
Nonfluent aphasia with impaired comprehension. Both Broca's and Wernicke's areas affected.
What happens in conduction aphasia? What areas affected?
Poor repetition but fluent speech, intact comprehension.
Arcuate fasciculus affected- connects Broca's and Wernicke's areas.
Draw a picture of the brain from the side, base, and a side cut. Label areas supplied by ACA, MCA, and PCA
Draw the circle of willis
What happens in an anterior spinal artery lesion?
Contralateral hemiparesis (lower extremities), medial leminiscus (decreased contralateral proprioception), ipsilateral paralysis of hypoglossal nerve.
What happens in PICA lesion
Lateral Medullary Syndrome (AKA Wallenberg;'s)- Contralateral loss of pain and temperature, ipsilateral dysphagia, hoarseness, decreased gag reflex, vertigo, diplopia, nystagmus, vomiting, ipsilateral horner's, ipsilateral facial pain and temperature, trigeminal nucleus, ipsilateral ataxia.
What happens in AICA lesion
Lateral Inferior Pontine Syndrome- Ipsilateral facial paralysis, Ipsilateral cochlear nucleus, vestibular, (nystagmus), ipsilateral facial pain and temperature, ipsilateral dystaxia (MCP, ICP)
What happens in a posterior cerebral artery lesion?
Contralateral homonymous hemianopia with macular sparing, supplied occipital cortex
Middle Cerebral Artery Lesion?
Contralteral face and arm paralysis and sensory loss, aphasia (dominant sphere), left sided neglect
Anterior Cerebral Artery Lesion?
Supplied medial surface of the brain. Leg-foot area of motor and sensory cortices
Anterior communicating artery lesion
Most common site of circle of willis aneurysm. Lesion may cause visual deficit.
Posterior Communicating Artery lesion
Common Area of aneurysm. Causes CN III palsy.
Lateral Striate Lesion
Division of middle cerebral artery, supply internal capsule, caudate, putamen, globus pallidus. Arteries of stroke. Infardct of the posterior limb causes pure motor hemiparesis.
Watershed Zones Lesion
Between anterior cerebral/ middle cerebral, posteior cerebral/ middle cerebral arteries. Damages in severe hypotension -> upper leg/ upper arm weakness, defects in higher order visual processing
Basilar Artery Lesion
Infarct causes locked in syndrome. CNII is typically intact.
Stroke of anterior circle generally causes?
General sensory and motor dysfunction and aphasia.
Stroke of posterior circle generally causes?
Cranial nerve deficits (vertigo, visual deficits), coma, cerebellar deficits (ataxia), dominant hemisphere (Ataxia), nondominant (neglect)
Where is most common location for a Berry Aneurysm? Complications? Associations? Risk Factors
Occurs at the bifurcation in the circle of willis. Most common site is bifurcation of the Anterior communicating artery. Rupture leads to hemorrhagic stroke/ subarachnoid hemorrhage. Associated with adult polycystic kidney disease, Ehler's Danlos Syndrome, and Marfan's Syndrome.

Other risk factors include advanced age, hypertension, smoking, race (higher in blacks)
What happens in an Epidural hematoma? Commonly ruptured artery? Secondary to? What will CT show?
Rupture of the middle meningeal artery, often secondary to fracture of temporal bone.Lucid Interval. Rapid expansion under systemic arterial pressure. Transtentoral herniation. CN III palsy.

CT will show biconvex disk, not crossing suture lines. Can cross falx, tentorium
What happens in a subdural hematoma? Seen in what populations/ circumstances? Predisposing factors?
Rupture of bridging veins. Slow venous bleeding. (Less pressure= hematoma develops over time) with delayed onset of symptoms. Seen in elderly individuals, alcoholics, blunt trauma, shaken baby.

Predisposing factors include brain atrophy, shaking, and whiplash.

Crescent-shaped hemorrhage that crosses suture lines. Gyri are preserved, since pressure is distributed equally. Cannot cross falx, tentorium.
What happens in subarachoid hemorrhage? What would you treat vasospasm with?
Rupture of an aneurysm (usually a berry aneuryms in Marfan's, Ehler's Danlos, APCKD) or an AVM.

Patients complain of worst headache of my life. Bloody or yellow (xanthochromatic) spinal tap. 2-3 days afterwards there is a risk of vasospasm due to blood breakdown products which irritrate vessels.

Treat with calcium channel blockers.
What is a parenchymal hematoma caused by? Typically occurs where
Caused by hypertension, amyloid angiopathy, Lobar strokes all over brain, diabetes melitis and internal capsule.
Stages of Irreversible Brain Damage
What areas are most vulnerable?
Irreversible Damage after 5 minutes. Irreversible neuronal injury (red neurons -12 to 48 hours), necrosis+ neutrophiles (24-72 hours), macrophages (3-5 days), reactive gliosis+ vascular proliferation (1-2 weeks), glial scar (>2 weeks)

Areas most vulnerable include hippocampus, neocortex, cerebellum, and watershed areas.
What happens in atherosclerosis?
Thrombi lead to ischemic stroke with subsequent necrosis (red neurons). Forms cystic cavity with reactive gliosis.
What happens in a hemorrhagic stroke? May be secondary to what?
Intracerebral bleeding, often due to aneurysm rupture. May be secondary to ischemic stroke following reperfusion (increases vessel fragility).
Ischemic Stroke? Causes? Lacunar strokes? Secondary to? Treatment?
Emboli block large vessels, etiologies include atrial fibrillation, carotid dissection, patent foramen ovale, endocarditis. Lacunar strokes block small vessels are secondary to hypertension. Treat with tPA within 3 hours.
What happens in a TIA?
Brief reversible episode of neurologic dysfunction due to focal ischemia. Symptoms last for < 24 hours.
How does stroke imaging for MRI vs CT compare.
Bridge on diffusion weighted MRI in 3-30 minutes and remains bright for 10 days.

Dark on CT in approximately 24 hours.
Explain flow of Dural Venous Sinuses.
Run in the dura matter where its meningeal and periostal layers seperate.

Cerebral veins-> venous sinuses -> Internal jugular veins.
Where is CSF made and desribe its pathway? Where is it reabsorbed?
CSF is made by the choroid plexus. From lateral ventricle to third ventricle via foramen of Monro to 3rd ventricle to 4th ventricle via cerebral aqueduct. Form the forth ventricle it goes to the subarachnoid space via the foramen of luschka (laterally) and foramen of magendie (medially). Reabsorbed by venous sinus arachnoid granulations.
What happens in Normal Pressure Hydrocephalus?
"Wet, Wobbly, Wacky". Does not result in increased subarachnoid space volume. Expansion of ventricles distorts the fibers of the corona radiata and leads to clinical triad of dementia, ataxia, and urinary incontinence (a reversible cause of dementia in elderly)
What happens in a communicating hydrocephalus?
Decreased CSF absorpiton by arachnoid villia which can lead to increased intracranial pressure, papilledema, and herniation (arachnoid scarring post meningitis
What happens in obstructive (noncommunicating hydrocephalus)
Caused by a structural blockage of CSF circulation within the ventricular system. (Ex. stenosis of aqueduct of sylvius)
What happens in hydrocephalus ex vacuo.
Appearance of Increased CSF in atrophy (Alzheimer's Disease, Advanced HIV, Pick's Disease). Intracranial pressure is normal. Triad is not seen.
How many spinal nerves are there? How many types of each?

What's special about C1-C7?

What happens in a vertebral disk herniation? Usually affects?
31 spinal nerves, 8 cervical, 12 thoracic, 5 lumbar, 5 sacral, 1 coccygeal.

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

Vertebral disk herniation (nucleus pulposis herniates through annulus fibrosis) usually occurs between L5 and S1.
Where does spinal cord extend in adults? What about subarachnoid space in adults?

Where is a lumbar puncture performed?
Spinal Cord- Lower Border of L1-L2
Subarachnoid Space- Lower border of S2

Usually performed at L3-L4 or L4-L5 interspaces at the level of the cauda equina. To keep the cord alive, keep the spinal needle between L3 and L5.
When doing a lumbar puncture, what are the spaces you will pass through?

At what level will you perform a lumbar puncture?
Skin/ Superficial Fascia, Ligaments (Supraspinous, Interspinous, Ligamentum flavum), Epidural Space, Dura mater, subdural space, arachnoid, and subarachnoid space.

The pia is not pierced!

At the level of the illiac crest between L4 and L5.
Draw spinal cord and associated tracks
Legs are lateral in lateral corticosional, spinothalamic tracts.

Dorsal column is organized as you are with hands at sids. Arms outside, legs inside
What is the Dorsal Column- Medial Lemniscus pathway responsible for?
Ascending pressure, vibration, touch, and proprioceptive sensation
Diagram Dorsal Column- Medial Lemniscus Pathway
1. 1st order neuron: Sensory nerve ending-> cell body in dorsal root ganglion-> enters pinal cords, ascends ipsilaterally in dorsal column-> synapses at nucleus cuneatus or gracillus in the medulla->
2. decussates in medulla-> ascends contralaterally in medial lemniscus-> synapses at VPL of thalamus-> and ends up at 3. sensory cortex
What is the spinothalamic tract responsible for?
Ascending pain and temperature sensation
Diagram spinothalamic tract
1. Sensory nerve ending (A-dlta and C fibers) (cell body in dorsal root ganglion)-> enters spinal cord-> ipsilateral gray matter of spinal cord->
2. Decusates at anterior white commissure and ascends contralterally-> VPL of thalamus->
3. sensory cortex
What is the lateral corticospinal tract responsible for?
Descending voluntary movement of contralteral limb
Diagram Lateral Corticospinal Tract
1. Upper Motor Neuron Cell Body in Primary motor cortex descends ipsilaterally through internal capsule until decussates at caudal medulla (pyramidal decussation and descends contralaterally) -> cell body of anterior horn (spinal cord)->
2. Lower motor neuron leaves spinal cord-> neuromusclar junction->
What are the signs you will see in an upper motor neuron lesion
Weakness, Increased reflexes, in creased tone, Babinksi, spastic paralysis, clasp knife spasticity

No change in atrophy, no fasciculations
What are the signs you will see in a lower motor neuron lesion?
Weakness, Atrophy, Fasciculation, Decreased reflexes, Decreased Tone

No babinksi, no spastic paralysis, no clasp knife spasticity
What is a fasciculation
Muscle twitching
What happens in Poliomyelitis? Caused by?
Caused by poliovirus which is transmitted by the fecal-oral route, Replicates in the oropharynx and small intestine before spreading through the bloodstream to the CNS where is leads to the destruction of cells in the anterior horn of the spinal cords, leading in turn to lower motor neuron destruction.
What are the signs and symptoms you will see in Poliomyelitis
Malaise, headache, fever, nausea, abdominal pain, sore throat, Signs of LMN lesions- muscle weakness, atrophy, fasciculations, fibrillations, and hyporeflexia

You will also find CSF with lymphocytic pleocytosis with slight elevation of protein (With no change in CSF glucose). Virus recovered from stool or throat)
Werdnig Hoffman Disease
Also known as infantile spinal muscular atrophy. Autosomal-recessive inheritance, presents at birth as a "floppy baby", tongue fasciculations, median age of death 7 months. Associated with degeneration of anterior horns. LMN involvement only.
Amyotrophic Lateral Sclerosis
Lou Gerig;s Disease. Associated with both LMN and UMN signs, no sensory, cognitive, or oculomotor deficits. Can be caused by defect in superoxide dismutase 1 (SOD1), betel nut ingestion. Commonly presents as fasciculations.
Tabes Dorsalis
Degeneration of dorsal columns and dorsal roots due to tertiary syphilis, resulting in impaired proprioception and locomotor ataxia. Associated with charcot's joints, shooting (lightning pain) (see image 12 in First Aid), Argyll Robertson upils (Reactive to accommodation but not light), absence of DTRs, positive romberg, and sensory ataxia at night.
Friedreich's Ataxia
Autosomal recessive trinucleotide repeat disorder (GAA, frataxin gene). Leads to impairment in mitochondrial functioning. Staggering gait, frequent falling, nystagmus, dysarthria, pes cavus, hammer toes, hypertrophic cardiomyopathy (Cause of death). Presents in childhood with kyphoscoliosis.
What happens in Brown Sequard Syndrome . What happens if lesion is above L1.
Hemisection of spinal cord.

You will see: ipsilateral UMN signs (corticospinal tract below lesion),

ipsilateral loss of tactile,
vibration, proprioception sense (Dorsal column below lesion),
Contralateral pain and temperature loss (spinothalamic tract) below lesion.

Ipsilateral loss of all sensation at level of lesion.
LMN signs (flaccid paralysis) at level of lesion.

If lesion occurs above T1, presents with Horner's syndrome.
What happens if you have complete occlusion of anterior spinal artery?
Spares dorsal column and tract of lissauer, upper thoracic ASA territory is a watershed area as artery of ademkiewicz supplies asa below T8.
What happens in Syringomyelia?
Damages anterior white commissure of spinothalamic tract (2nd-order neurons) resulting in bilateral loss of pain and temperature sensation (usually C8-T1) seen with arnold Chiari I, can expand and affect other tracts
What part of spinal cord is damaged in friedrich's ataxia, vitamin B12 neuropathy, and vitamin E deficiency
Demyelination of dorsal columns, lateral corticospinal tracts, and spinocerebellar tracts, ataxic gait, hyperreflexia, impaired position and vibration sense
What happens to spinal cord in Multiple Sclerosis
Mostly white matter of cervical region is affected. Random and asymmetric lesions due to demyelination.
Scanning speech, intention tremor, and nystagmus,
What happens in Horner's Syndrome?
Sympathectomy of face:
1. Ptosis (slight drooping of eyelid)- superior tarsal muscle)
2. Anhidrosis (absence of sweating) and flushing (rubor) of affected side of face
3. Miosis (pupil constriction)

Associated with lesion of spinal cord above T1 (Pancoast's tumor, Brown-sequard syndrome [cord henisection], late-stage syringomyelia.
What is the 3 neuron oculosympathetic pathway.
Projects from hypothalamus to intermediolateral column of spinal cord then to superior cervical (sympathetic ganglion) and finally to the pupil, smooth muscle of eyelids, and the sweat glands of the forehead and face.

Interruption of any of these pathways results in Horners syndrome.
Approximately where are these dermatomes located: C2, C3, C4, T4, T7, T10, L1, L4, S2, S3, S4
C2- posterior half of a skull cap
C3-high turtleneck shirt
C4- low-collar shirt
T4- at the nipple
T7- at the xiphoid process
T10- at the umbilicus (important for early appendicitis pain referral)
L1- inguinal ligament
L4- includes the kneecaps
S2,S3,S4- erection and sensation of penile and anal zones.
Diaphragm and gallblader pain referred to where via?
Referred to shoulder via phrenic nerve.
How do muscle spindles work?
In parallel with extrafusal muscle fibers. Muscle stretches-> intrafusal stretch-> simulates 1a afferent-> dorsal horn -> stimulates alpha motor neuron-> reflex muscle (extrafusal contraction)

Muscle spindles monitor muscle length (help you pick up a heavy suitcase when you didn't know how heavy it was)
How do golgi tendons work
Series to intrafusal muscle-> Ib afferent which inhibits alpha motor neuron
Golgi tendon organs monitor muscle tension and prevent tendon tear (make you drop a suitcase you've been holding too long).
How does gamma loop work?
CNS stimulates gamma motor neuron which contracts intrafusal fiber at central part of muscle spindle which increases sensitivity of reflex arc. Can be influenced by the brain.
Where are the clinical reflexes? What nerve roots innervate these clinical reflexes?

Biceps= C5
Triceps =C7
Patella= L4 nerve root
Achilles= S1 nerve root

Babinski- dorsiflexion of the big toe and fanning of other toes, sign of UMN lesion, but normal reflex in first year of life
Moro Reflex?
Hang on for life reflex- abduct/ extend limbs when startled and then draw together
Rooting Reflex
Movement of head toward one side of check or mouth if stroked (nipple seeking)
Sucking Reflex
Sucking response when roof of mouth is touched
Palmar and Plantar Reflex
Curling of finger/toes if palms of hands/feet are stroked
Babinski Reflex
Dorsiflexion of large toe and fanning of other toes with plantar stimulation
When do reflexes disappear? When might they reappear
Disappear during first year of life.

Might reappear with a frontal lobe lesion.
What CNs lie medially at the Brain Stem?
3, 6, 12
What is the pineal gland responsible for?
Melatonin secretion, circadian rhythms
What is the superior colliculi responsible for?
Conjugate verticle gaze center
Inferior colliculi?
What is parinaud syundrome
Paralysis of conjugate vertical gaze due to lesion in superior colliculus (pinealoma)
Label the brain stem
CN 1
Olfactory, Smell (Only CN without thalamic relay to cortex), Sensory
CN 2
Optic, Sight, Sensory
CN 3
Occulomotor, Eye movement (SR, IR, MR, IO), pupillary constriction (PS: E-W nucleus, muscarinic R) accomodation, eyelid opening (levator palpebrae), Motor
Trochlear, Eye movement (SO), Mo
Trigeminal, Mastication, facial sensation (opthalmic, maxillary, mandibular divisions), Sensory and Motor
Abdducens, Eye Movement (LR), Motor
Facial, Facial movement, taste from anterior 2/3 of tongue, lacrimation, salivation (submandibular and sublingual glands), eyelid closing (orbicularis oculi), stapedius muscle in ear, sensory and motor
Occulomotor Hearing, Balance, Sensory
Glossopharyngeal, Taste from posterior 1/3 of tongue, swallowing, salivation, parotid gland, monitoring carotid body and sinus chemo- and baroreceptors and stylopharyngeus (elevates pharynx and larynx, sensory and motor
Vagus, Taste from epiglottic region, swallowing, palate elevation, midline uvula, talking, coughing, thoracoabdominal viscera, monitoring aortic arch chemo and baroreceptors, both
Accessory, Head turning, shoulder shrugging (SCM, Trapezius)
Tongue Movement, Motor
Where are the cranial nerve located?
Tegmentum portion of brainstem (between dorsal and ventral portions)
What cranial nerves are located in the midbrain
Nuclei of CN III AND IV
What cranial nerves are located in the pons
Nuclei of CN V, VI, VII, VIII
What cranial nerves are located in the Medulla
Nuclei of IX, X, XI, XII
What does sulcus limitans do?
Divides sensory alar plate (lateral nuclei) from motor basal plate (medial nuclei)
Corneal Reflex?
Afferent- V1 (opthalmic- nasociliary branch, levator palpebrae)

Efferent- VII (Temporal Branch, Orbicularis Oculi)
Afferent- V1 (loss of reflex does not preclude emotional tears)

Efferent- VII
Jaw Jerk
Afferent:V3 (sensory- muscle spindle from masseter)

Efferent: V3 (motor-masseter)
Afferent- II

Efferent- III
Afferent- IX

Efferent- IX, X
What are the three vagal nuclei
Nucleus Solitarius
Nucleus Ambiguus
Dorsal Motor Nucleus
Nucleus Solitarius
Visceral Sensory Information (taste, baroreceptors, gut distention), CN VII, IX, X
Nucleus Ambiguus
Motor innervation of pharynx, larynx, upper esophagus (swallowing, palate elevation), CN IX, X, XI
Dorsal Motor Nucleus
Sends autonomic (parasympathetic) fibers to heart, lungs, and upper GI.
Where is CN I located?
Cribiform Plate
Where are cranial nerves II- VI located?
Middle cranial fossa through sphenoid bone.
What is located in the optic canal
CN II, Opthalmic Artery, Central Retinal Vein
What is located in the superior orbital fissue
CN III, CN IV, CN V1, VI, opthalmic vein, sympathetic fibers
What is located in the foramen Rotundum
What is located in the Foramen Ovale>
What is located in the foramen spinosum?
The middle menigneal artery
Mnemonic for remembering Divisions of CN V locations
Standing Room Only
Superior Orbital Fissure, Rotundum, Ovale
Where are cranial nerves VII-XII located
Posterior cranial fossa through temporal or occipital bone
What is located in the internal acoustic meatus?
What is lcated in the jugular foramen
CN IX, X, XI, Jugular vein
What is located in the hypoglossal canal
What is located in the foramen magnum?
Spinal roots of CN XI, brain stem, vertebral arteries
Cavernous Sinus. What nerves run through it? Which one is free floating?
A collection of venous sinuses on either side of the pituitary. Blood from eye and superficial cortex-> cavernous sinus-> internal jugular vein.

CN III, IV, V1, V2, and VI and postganglionic sympathetic fibers en route to the orbit all pass through the cavernous sinus. Only CN VI is free floating. Cavernous portion of internal carotid artery is here.

Nerves that control extraocular muscles plus V1 and V2 pass through)
Cavernous Sinus Syndrome Signs
Due to mass effect- opthalmoplegia, opthalmic and maxillary sensory loss
What happens in a CN XII LMN lesion?
Tongue deviates toward side of lesion (lick your wounds) and decussates before medullar and synapses on contralateral hypoglossal nucleua.
What happens in a CN V motor lesion
Jaw deviates toward side of lesion. Bilateral cortical input to the pterygoid muscle.
What happens in a CN X lesion
Uvula deviates away from side of lesion. Weak side collapses and uvula points away.
What happens in a CN XI Lesion-
Weakness turning head to contralateral side of lesion. Shoulder droop on side of lesion (trapezius)
What happens in UMN lesion of facial nerve
Lesion of motor cortex of connection between cortex and facial nucleus.

Contralteral paralysis of lower face only, since upper face recieves bilateral UMN innervation
What happens in a LMN lesion
Ipsilateral paralysis of upper and lower face
What happens in Bell's Palsy
Complete destruction of the facial nucleus itself or its branchial efferent fibers (facial nerve proper)

Peripheral ipsilateral facial paralysis with inability to close eye on involved side

Can occur idiopathically, gradual recovery in most cases
What can Bell's Palsy be a complication from
AIDS, Lyme disease, Herpes Zoster, Sarcoidosis, Tumors, Diabetes

ALexander graHam BELL with STD
What does kuh-kuh-kuh test?
Palate elevation- CN x- VAGUS
What does La La La Test?
Tests Tongue, Hypoglossal, CN XII
What does mi mi mi test?
Tests lips CN VII
What are the muscles of mastication? Which ones close and which ones open? Innervated by
3 muscles close jaw:masseter, temporalis, medial pterygoid (Takes more muscles to keep your mouth shut)

1 Opens:lateral pterygoid. (Lateral Lowers)

All are innervated by trigeminal nerve (V3)
Muscles with glossus in their name are innervated by? Exception
Innervated by Hypoglossal nerve, Palatoglossus is the exception (Vagus nerve)
Muscles with palat in their name are innervated by? Exception
Innervated by vagus nerve.

Exception: Tensor Veli Palatini innervated by mandibular branch of CN V
What does the inner ear consist of?
Consists of a series of tubes in the temporal bone (bony labrinth) filled with perilymph (Na+ rich, similar to ECF)that includes cochlea, vestibule, and semicircular canals.
What is within the bony labyrinth
2nd series of tubes (membranous labyrinth) filled with endolymph (K rich, similar to ICF) that includes cochlear duct (within the cochlea), utricle and saccule (within hte vestibule), and semicircular cannals.

Hair cells (located within the organ of corti are the sensory elements in both vestibular apparatus (spatial orientation) and cochlea (hearing)
Endolymph is made by?
Stria Vascularis
What do the utricle and saccule contain? What do they detect? Which is vertical which is horizontal?
Contains maculae- detects linear acceleration.

Utricle is horizontal, saccule is verticle.
Semicircular canals contain? What do they detect
Contain Ampullae, detect angular acceleration.
Explain frequencies and wavelengths and different parts of the cochlea
At base, high frequency, low wavelength

At apex- high wavelength, low frequency
Hearing loss in the elderly?
High frequency sounds than low frequency sounds as hearing loss progresses
What happens as sound enters the middle ear?
Vibration of tympanic membrane > ossicles-> oval window-> vibration of basilar membrane-> bending of hair cilia against tectorial membrane-> hair cell bending= hyper or depolarization of CN VIII
Which is heard better in a normal person? Bone conduction or air conduction
Air conduction > Bone Conduction
What happens if Bone conduction is greater than air conduction?
Conduction deafness in that ear. Weber lateralizes to that ear.
What happens if AC>BC
Normal, but there is sensorineural loss. Weber lateralizes to opposite ear.
What happens in retinitis
Retinal necrosis+ edema-> atrophic scar
What happens in irritis?Example of a disease?
Systemic inflammation, Reiters
Near Vision
Ciliary muscle contracts, zonular fibers relax, lens relaxes, more convex
What happens in distant vision
ciliary muscle relaxes and lens flatten
What happens to the eye in aging
Sclerosis and decreased elasticity causes lens shape to change.
What happens in a retinal artery occlusion
Acute painless monocular loss of vision, pale retina and cherry-red macular (has its own blood supply- choroid artery)
Draw anatomy of the eye
Draw aqueous humor pathway plus surrounding structures
What is dilator/radial muscle activated by? causes?
A1 stimulation, mydriasis
What is sphincter/circular constrictor muscle innervated by
M3-> meiosis
What activates Ciliary process? produces?
B stimulation, produces aqueous humor
What does ciliary muscle activated by? results in
M3, accomodation
What happens in glaucoma? What are the types of glaucoma?
Imapired flow of aqueous humor-> increased intraocular pressure-> optic disk atrophy with cupping.

Open (wide) and closed
(narrow) angle
Open/Wide Glaucoma, mostly affects
Obstructed outflow (Canal of schlemm) associated with myopia, increase in age, African American race, more common, silent ,painless
Closed/ Narrow Angle- What do you know what to give in this case
Obstruction of flow between iris and cornea-> pressure buildup behind iris. Very painful, decreases vision, rock-hard eye, frontal headache. Opthalmologic emergency.

Do not give epinephrine!
What is a cataract? Risk factors
Painless, bilateral opacification of lens, decrease in vision.

Risk factors include age, smoking, etoh, sunlight, classic galactosemia, galactokinase deficiency, diabetes (sorbitol), trauma, and infection
What is papilledema?
Increase in intracranial pressure which causes elevated optic disk with blurred margins, bigger blind spot (can be seen in hydrocephalus)
What happens in CN III Damage?
Eye looks down and out, ptosis, pupillary dilation, loss of accommodation
What happens in CN IV damage?
Diplopia with a defective downward gaze (adjust be tilting head toward lesion)
What happens in a CN VI lesion
Medially directed eye
What does superior oblique do while adducted
Abducts, Intorts and depresses
Describe anatomy of orbit of eye when eye is removed.
Draw eye testing diagram
IOU- to Test Inferior Oblique have patient look inward and up
Misalignment of eyes. Multiple etiologies
Reduction of vision from disuse in critical period. May be secondary to strabismus, deprivation, unequal refractive errors
What causes constriction of pupils
Pupillary sphincter muscle (aka circular muscle)
What causes parasympathetic innervation of pupils
Innervation CN III from Edinger-Westphal nucleus -> ciliary ganglion
What causes dilation of pupils. Draw pathway
Radial muscle (aka pupillary dilator muscle), sympathetic. Innervation- T1 preganglionic sympathetic-> superior cervical ganglion-> postganglionic sympathetic-> long ciliary nerve
Explain pupillary light reflex
Light in either retina sends a signal via CN II to pretectal nuclei (dashed lines) in the midbrain that activates bilateral edinger-westphal nuclei, pupils contract bilaterally (consensual reflex)

Result: illumination of 1 eye results in bilateral pupillary constriction
What is a marcus Gunn Pupill-
Afferent pupillary defect (due to optic nerve damage or retinal detachment. Decreased bilateral pupillary constriction when light is shone in affected eye.
What happens in retinal detachment? Causes?
Separation of neurosensory layer of retine from pigment epithelium-> degeneration of photoreceptors -> vision loss. May be secondary to trauma, diabetes.
What happens in Age related macular degeneration? What are the types?
Degeneration of macula (Central area of retina). Causes loss of central vision (scotoma)

Dry/ Atrophic ARMD is slow, due to fat deposits and causes gradual decrease in vision

Wet ARMD is rapid, due to neovascularization.
Draw the different visual field defects that can occur?
What happens to an image when it hits the primary visual cortex?
It is upside down and left-right reversed.