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Terms in this set (84)
What to think of with brief duration of symptoms?
What to think of with relapsing of symptoms?
What to think of with sudden onset or fixed deficit of symptoms?
What to think of with slow progressive symptoms?
Parkinson's or Brain tumor
Damage in one area (brain tumor or stroke)
Focal damage at multiple sites (MS)
Widespread (metabolic issue/Structural)
Speech (dominant hemisp)
Primary sensory cortex
Sensory INTEGRATION (organize sensations from parietal lobe and make use of it)
Taste and smell
Primary visual cortex
Broca's area damage
Expressive aphasia. Comprehension intact but unable to speak to varying degrees
Wernicke's area damage
Receptive aphasia. Comprehension not intact; fluent but nonsensical speech. (stroke, trauma, and mass lesions)
Inability to recognize sensory stimuli. (olfactory, auditory, visual, etc.) Associated with large parieto-occipital-posterior temporal lesion. (stroke or dementia)
Movement (arm swing during walking, etc.)
Primary sensory relay
CN III and IV
Motor information (voluntary)
UMN originate in pre-central gyrus. Cross to contralateral side in medulla.
Descends ipsilaterally (synapse in anterior horn)
Carry light touch, pain, temp & pressure.
Crosses immediately in the spinal cord
Vibration, proprioception, and discriminative touch
DOES NOT CROSS UNTIL IT GETS TO MEDULLA
Olfactory groove meningioma symptoms
Hyposmia, anosmia, difficutly with concentration (frontal lobe involvement)
CN III (olfactory)
Pupillary reflex (CN II & III)
Extraocular muscles (LR6SO4)
Pitutary tumor symptoms
CN II deficit!! (BITEMPORAL HEMIANOPSIA)
Increased growth hormone - acromegaly
Increased prolactin - Infertility, galactorrhea, amenorrhea
Increased adrenocorticotropic hormone (ACTH) - Leads to cushing's disease.
Lack of temporal vision in both eyes
LEsion at optic chiasm
Lack of temporal in one eye and nasal visual field in other eye.
Lesion at Optic tract.
CN IV (trochlear) innervation
Superior oblique (in and down)
CN VI (abducens) innervation
Sensation to face
Muscles of mastication
Corneal reflex (sensory)
CN VII (facial) innervation
Muscles of facial expression
Sensation to anterior 2/3 of tongue
Corneal reflex (motor)
Central CN VII lesion
Contralateral (opposite side of lesion) paralysis of lower face
Peripheral CN VII lesion (Bell's Palsy)
Ipsilateral paralysis of ENTIRE side of face.
Benign overgrowth on CNVIII associated with sensoineural hearing loss (SNHL)
Peripheral CNVII lesion.
Cerebellar ataxia(lack of voluntary motor control) with large lesions
Glossopharyngeal (CN IX)
Pharynx (motor) - Gag reflex
Sensation to post. 1/3 of tongue
Deviation of palate AWAY form lesion upon injury.
Loss of gag reflex
Vagus (CN X)
Pharynx and larynx (sensory)
Spinal acessory (CN XI)
Movemento fhead and shoulders (SCM and traps)
Hypoglossal (CN XII)
Tongue movement (speech)
Deviation TOWARDS lesion upon injury
What are the relexes?
Biceps (C5, 6)
Achilles (S1, 2)
Weakness - Spasticity
DTR - INcreased
Babinski - POSITIVE
Atrophy - Absent
Fasciculation (small focal contraction) - Absent
DTR - Decreased/absent
Babinski - absent
Atrophy - increased
Fasciculations - Present
Spinal cord compression
C6 (six shooter)
Middle finger dermatome
Fifth digit dermatome
Trunk dermatome (nipple line)
Anterior thigh dermatome
Anterior shin dermatome
Top of foot dermatome
Bottom of foot dermatome
T10 cord lesion (complete)
Motor- Spastic parplegia
Sensory - Loss of sensation in BLE
DTRs - Knee and ankle jerks +3 (excessive).
Brown-Sequad lesion (right hemisection of cord, right T10)
Motor- RLE plegia (disruption or corticospinal tract).
Sensory - Decrease vibration and prorpioception on RLE (disruption of posterior columns on right). Decreased light tough and pinprick on LLE (disruption of spinothalamic tract on right)
Sensation - Decreased LT/PP in BLE in stocking distrib. Vibration absent at great toe, present but diminished at medial malleolus.
DTRs - 1+ and symmetric at knees and absent at both ankle; toes are downgoing bilaterally.
Foramen of Monroe
Aquaduct of sylvius
Foramina of Magenda & Luschka
MIdline & Lateral
Seizures - Pathophysiology
Paroxysmal event characterized by abnormal neuronal discharges
Seizures - Etilogy
Stroke, infection , tumors, degen. disease, trauma.
Simple partial seizure (SPS)
Consciousness preserved. May be motor, sensory or autonnomic.
Jacksonian march with motor.
Can have post-ictal paresis (weakness)
Complex-partial seizure (CPS)
Automatisms - Semi- purposeful movement or vocalizations (humming, lip smacking, etc.)
Treatment for CPS and SPS
Carbamazepine (Tergetol), phenytoin (Dilantin), valproate (Depakene)
Absence seizures - Signs and symptoms
Brief interruption of consciousness.
Staring, rythmic eye blinking, and automatisms.
Absence seizures - Treatment
Ethosuximide (Zarontin), Valproic acid (Depakene), Lamotrigine (Lamictal)
Generalize Tonic-Clonic seizures - Signs/Symptoms
Loss of consciousness
Respiratory arrest follows
Muscles rigidity (tonic)
1-2 min of rhythmic muscle contrac (clonic)
Cyanosis, toungue-biting, incontinence
Post-ictal confusion & somnolence.
Generalize tonic clonic seizures - Treatment
Status Epilepticus - Signs/Symptoms
More than 20 minutes of seizure activity
Two or more sequential seizures without full recovery of consciousness
Status Epilepticus - Treatment
IV benzos (control seizure)
Load w/Phenytoin (antiepileptic)
Add phenobarbitol if needed (sedative)
Continuous EEG monitoring looking for burst suppression
Multiple Sclerosis - Epidimiology
Women > men
Higher risk in caucasian
Multiple Sclerosis - Etiology
Multiple Sclerosis - Dx
Identify two events occuring over different periods of time and separated by at least one month; affecting distinct anatomic regions.
Multiple sclerosis - Symptoms (HPI)
Bilateral trigeminal neuralgia
Multiple Sclerosis - Signs (physical exam)
Intranuclear ophthalmoplegia (INO) - Bilateral impair. w/ adduct.
Multiple sclerosis - Disease progression
Relapsing/remitting - Discrete attacks w/ almost complete rcovery
Primary progressive - Gradual decline and onset of sypmtoms
Secondary progressive - Fewer relapses associated w/ increasing disability.
Progressive/relapsing- Steady decline from onset with occasional superimposed attacks
Multiple sclerosis - Dx
CSF: Icreased, IgG, oligoclonal bands
MRI: Periventricular white matter (plaques) - Demyelination
Evoked potential consistent with abnormal conduction (slowed nerve signals)
Multiple Sclerosis - Treatment of acute exacerbations
Corticosteroids (decrease inflamm.) - Methylprednisone daily X3-7 days
Multiple Sclerosis - Disease modifying treatment
Dcrease # of relapses, reduce progression, decrease number of lesions on MRI
Beta interferon (Betaseron, Avonex, Rebif)
Multiple Sclerosis - Symptom based treatment
Fatigue - amantidine (Symmetrel)
Spasticity - baclofen (Lioseral)
Urgency - Anticholinergice - betanechol (Urocholine)
Neuralgia - carbamazepine (Tegretol)
Tremor - proanolol (Inderal)
Depression - SSRIs: fluoxetine (Prozac), sertraline (Zoloft), citalopram (Celexa)
Parkinson's Disease - Pathophysiology
Degeneration of substantia nigra leading to decreased dopamine.
Parkinson's disease - Symptoms (HPI)
Slowness of movements
Resting tremor (pill rolling)
Dementia in 30%
Parkinson's disease - Signs
Bradykinesia (slow to get going)
Assymmetric resting tremor
Parkinson's disease - Dx
No diagnostic criteria. R/O other diseases first
Parkinson's disease - Treatment
Levadopa/Carbidopa (Sinemet) - Wearing off phenomnon within 5-10 yrs (dystonia and dyskinesia)
Bromocriptine (Parlodel), pergolide (Permax), ropinirole (Requip), pramipexole (Mirapex)
MAO-B inhibitors: Selegilene (Eldepryl)
Indirect dopamine agonists - Amantadine (Symmetrel)
Anticholinergics - Used when tremor is predominant symptom. YOUNGER PATIENTS (these are bad in older pts because of SEs)
EX: Trihexylphenidyl (Artane)
Surgery: Relieve motor fluctuations, dyskinesias, or debilitating tremor. Deep brain stimulation (DBS).
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