Pance Pearls: Neuro Flashcards
4 lobes of the brain=
Frontal, parietal, temporal, occipital
Involuntary spasms or repetitive motions or abnormal voluntary movement
Dyskinesia
Sustained contraction (muscle spasm) esp of antagonistic muscles (ex simultaneous biceps and triceps contraction); twisting of body, abnormal posturing (ex torticollis, writer’s cramp)
Dystonia
Sudden brief sporadic single repetitive jerks/twitching of 1 muscle or muscle group (not suppressible)
Myoclonus
Sudden repetitive nonrhythmic movements or vocals using specific muscles groups (suppressible unlike myoclonus): Ex. tourette’s syndrome
Chorea
Muscle contractions; Tonic (prolonged sustained contraction/rigidity); Clonic (repetitive rapid movement)
Muscle spasms
Rhythmic movement of a body part
Tremors
Tremor at rest (ex. Parkinson’s)
Resting tremor
Tremors occurring while holding position against gravity
Postural tremor
Tremor occurring during moment or when nearing a target
Intentional tremor
Disorder associated with tremor, bradykinesia, rigidity, and postural instability
Parkinsonism
Loss of the dopamine producing cells of the substantia nigra (in basal ganglia)
Parkinsonism
Medications that block dopamine (dopamine antagonists)- ex. typical and atypical antipsychotics can cause this=
Parkinsonism
Disease with loss of anticholinergic neurons (similar to alzheimer’s) where the pt develops dementia and loss of dopaminergic neurons (sharing symptoms similar to Parkinson’s disease)
Lewy Body Dementia
Autosomal dominant inherited disorder or unknown etiology; onset of age usually in 60s; may begin at any age, worsened with emotional stress & intentional movement;; Tremor shortly relieved with alcohol ingestion; On finger to nose test, tremor increases as target approached; MC in upper extremities (usually spares legs)
Essential familial tremor
May be used to treat Essential familial tremor if severe:
Propranolol
Idiopathic dopamine depletion-> failure to inhibit acetylcholine in basal ganglia (Ach is excitatory CNS neurotransmitter, dopamine is INHIBITORY); Cytoplasmic inclusions (Lewy Bodies) & loss of pigment cells seen in substantial nigra (which produces dopamine)
Parkinson’s Disease
Classic: tremor, bradykinesia, rigidity with progressive postural instability (often occurs in ages 45-65)
Parkinson’s Disease
In Parkinson’s disease, worse at rest, emotional stress (lesseTened with voluntary activity/intentional movement & sleep); often first symptom; usually confined to one limb or one side for years before it becomes generalized
Tremor
MC sign in Parkinson’s disease
Resting tremor (“pill-rolling” tremor)
In Parkinson’s disease; slowness of voluntary movement & decrease in automatic movements: lack of swinging of arms while walking/shuffle gait
Bradykinesia
In Parkinson’s, increased resistance to passive movement (flexed posture); Festination (increased speed while walking); normal DTR; usually no muscle weakness
Rigidity
Signs include relative immobile face (fixed facial expressions), widened palpebral fissures, seborrhea of skin is common; Decreased blinking
Parkinson’s disease
In Parkinson’s, tapping the bridge of the nose repetitively causes a sustained blink
Myerson’s sign
Most effective tx in Parkinson’s disease
Levodopa/Carbidopa (Sinemet)
_____ is converted to dopamine
Levodopa
______ reduces the amount of levodopa needed reducing SE of the levodopa
Carbidopa
Bromocriptine, Pramiprexole, Ropinirole; directly stimulate dopamine receptors; Less SE than levodopa; sometimes used in young pts to delay use of levodopa
Dopamine agonists
Blocks excitatory cholinergic effects; indicated in pts
Anticholinergics
Increases presynaptic dopamine release & improves long term levodopa-induced dyskinesias
Amantadine
Autosomal dominant neurodegenerative disorder; the gene causes neurotoxicity, cerebral & caudate nucleus atrophy; Symptoms appear after 30yrs of age; usually fatal
Huntington Disease
Initial symptoms are behavioral changes (personality, cognitive intellectual, psych), chorea (atrophy of caudate nucleus in basal ganglia) & dementia; Chorea is rapid, involuntary or arrhythmic movement of the face, neck, trunk & limbs initially; may have facial grimacing, ataxia
Huntington disease
Diagnose by CT scan: shows cerebral and caudate nucleus atrophy
Huntington disease
Onset usually childhood (2-5y) & may be associated with obsession compulsions (50% have resolution of symptoms by 18yrs); Motor tics of face, head, and neck (blinking, shrugging, head thrusting, sniffling)
Tourettes syndrome
May include verbal/phonetic tics ex. grunts, throat clearing, obscene words (coprolalia), repetitive phrases, repeating phrases of others (echolalia), self-mutilating
Tourette syndrome
Can be managed with Dopamine blocking agents or Alpha-adrenergics
Tourette syndrome
Acute/subacute inflammatory demyelinating polyradiculopathy with symmetric LOWER–> UPPER extremity weakness (ASCENDING WEAKNESS)
Guillian Barre Syndrome
Increased incidence with Campylobacter (MC) or other antecedent respiratory or GI infections, CMV, EBV, immunizations, surgery
Guillian Barre Syndrome
Immune-mediated demyelination & axonal degeneration slows impulses –> symmetric weakness & paresthesias; thought to be secondary to post-infection immune responses which cross-reacts with peripheral nerve components (molecular mimicry)
Guillian Barre Syndrome
Symptoms include weakness and paresthesias (usually symmetric); Decreased DTR; tachycardia, hypotension/hypertension, breathing difficulties
Guillian Barre Syndrome
Dx by CSF with high protein & normal WBC count (albuminocytological dissociation)–> may be d/t altered nerve capillary-CSF barrier defect
Guillian Barre Syndrome
Procedure done early in Guillian Barre Syndrome; removes harmful circulating Autoantibodies that causes the demyelination
Plasmapheresis
Tx of Guillian Barre; suppresses harmful inflammation/autoantibody & induces remyelination
IV immune globulin (IVIG)
Autoimmune disorder of the peripheral nerves; 75% have thymic abnormality (hyperplasia or thymoma) or other autoimmune disorders; MC in young women (HLA-DR3)
Myasthenia Gravis
Inefficient skeletal muscle neuromuscular transmission d/t autoimmune Ab against Ach (nicotinic) post synaptic receptor @ NMJ (decrease Ach receptors)–> progressive weakness with repeated muscle use and recovery after periods of rest
Myasthenia Gravis
Clinical manifestations include extra ocular muscle weakness–> diplopia; ptosis (eyelid weakness more prominent with upward gaze); pupils spared
Myasthenia gravis
Generalized muscle weakness; least in the morning worsened with repeated muscle use throughout day (relieved w/ rest), fluctuation; bulbar (orapharyngeal) muscle weakness (weakness w/ prolonged chewing, dysphagia) ; Respiratory muscle weakness (leading to respiratory failure)
Myasthenia Gravis
Test for Guillian Barre; rapid response to short acting IV edrophonium
Edrophonium (Tension test)
Dx with + Ach-receptor Antibodies; + muscle specific tyrosine kinase Ab
Myasthenia Gravis
Increases acetylcholine by decreasing acetylcholine breakdown
Acetylcholinesterase inhibitors
Associated with small cell lung CA, develop Ab preventing Ach release; weakness is improved with continued use
Myasthenia
Autoimmune inflammatory demyelinating disease of the CNS idiopathic origin with axon degeneration of white matter of the brain, optic nerve & spinal cord; MC in young adults (women) 20-40; associated with CNS IgG production abnormal T lymphocyte reaction
Multiple Sclerosis
MC type of Multiple sclerosis=
Relapsing-remitting disease (RRMS)
Clinical manifestation includes optic neuritis* (retrobulbar)-unilateral eye pain worse w/ eye movements, diplopia, scotoma/vision loss (esp color), blurry vision
Multiple sclerosis
In Multiple Sclerosis; both pupils constrict when you shine light into the normal eye but pupil’s “DILATE” when you quickly shone the light into the affected eye (response d/t brain perceiving the delayed conduction of affected optic nerve as if light was reduced)
Marcus Gunn pupil
Clinical manifestations include sensory deficits; weakness, parasthesisas, fatigue (75%); muscle cramping (spasticity); Uhthoffs’s phenomenon (worsening of sx w/ heat; pain, numbness, paresthesias in a limb, muscle cramping) & Lhermitte’s sign (neck flexion causes lighting-shock pain radiating from the spine down the leg)
Multiple sclerosis
Includes spinal cord sxs: bladder, bowel, or sexual dysfunction; Charcot’s neurological triad(nystagmus, staccato speech & intentional tremor); Spasticity & positive (upwards) babinski*
Multiple Sclerosis
Test of choice to confirm dx of Multiple Sclerosis
MRI* w/ gadolinium
MRI will show white matter plaques* (hyperdensistites)
Multiple Sclerosis
CSF will show increase IgG (oligoclonal bands)-sm, discrete bands in the gamma globulin seen on electrophoresis, which reflecting inflammatory cells penetrate the blood brain barrier)
Multiple Sclerosis
CSF revealing ‘High IgG (oligoclonal) bands’
Multiple Sclerosis
CSF revealing ‘High protein with NORMAL WBC cell count’
Guillian Barr Syndrome
CSF revealing ‘High protein with INCREASED WBC (polymorphonuclear neutrophils), DECREASED glucose*’
Bacterial Meningitis
CSF revealing ‘Normal glucose, Increased WBC lymphocytes’
Aseptic Viral Meningitis
CSF revealing ‘Increased WBCs (lymphocytes) and decreased glucose’
Fungal Meningitis
An acute, abrupt confused state (transient global disorder of attention) usually as a result of systemic problems with rapid onset and fluctuating mental status changes; Marked deficit in short term memory; usually 1 week with full recovery in most cases
Delirium
Progressive, chronic deterioration of selective functions; MEMORY LOSS and loss of impulse control, motor & cognitive functions NOT d/t delirium, medications, or psychiatric illness
Dementia
MC type of dementia; Loss of brain cells, amyloid deposition (senile plaques) in the brain, neurofibrillary tangles (tau protein); cholinergic deficiency–> memory, language, visuospatial changes; CEREBRAL CORTEX ATROPHY on CT scan*
Alzheimer’s disease
Used to manage Alzheimer’s disease; reverses cholinergic deficiency, may not always slow down progression of dz but helps with sx
Acetylcholinesterase inhibitors (Donepezil, Rivastigmine, Galantamine)
Used to manage Alzheimer’s disease; blocks NMDA receptor, slowing calcium influx and nerve damage; Glutamate is excitatory receptor–this reduces Glutamate’s excitotoxicity
NMDA antagonists
2nd MC type of Dementia; brain dz d/t chronic ischemia and multiple infarctions (ex. lacunar infarcts**); assoc w/ HTN
Vascular Dementia
Type of dementia; Rare; Localized brain degeneration of the frontotemporal area may progress globally; marked personality changes*; aka Pick’s disease
Frontotemporal Dementia
Abnormal protein deposits (Lewy bodies) in nerve cells; Visual hallucinations, delusions, Parkinsonism
Diffuse Lewy Body disease
Rapid dementia d/t prions
Creutzfeldt-Jakob dz
Predominantly middle-aged males with severe UNILATERAL periorbital/temporal pain (sharp, lacinating)* bouts lasting
Cluster headaches
Physical exam reveals IPSILATERAL Horner’s syndrome (ptosis, miosis, anhydrosis)*, nasal congestion/rhinorrhea, conjunctivitis & lacrimation
Cluster Headaches
First line tx in cluster headaches=
100% O2
Prophylaxis tx for cluster headaces=
Verapamil
MC in females; 2 types (w/ and w/o auras); Family hx 80%; Thought to be caused by vasodilation of the blood vessels innervated by the trigeminal nerve; Neuro findings d/t internal carotid constriction
Migraine headaches
Lateralized, pulsatile/throbbing headaches associated with N/V, photophobia & photophobia for 4-72 Hr duration; worse w/ physical activity, stress, lack/excessive sleep, ETOH, certain foods, OCPs/menstruation
Migraine headaches
Bilateral* tight band-like, constant daily HA worsened w/ stress, fatigue, noise, or glare (NOT ACTIVITY); usually not pulsatile; NO N/V or focal neurologic sx
Tension headaches
Compression of trigeminal nerve root (by superior cerebellar artery or vein); Brief episodic, stabbing/lancinating pain in the 2nd/3rd division of the Trigeminal nerve (CN V) worse with touch, eating, drafts of wind, and movements (often unilateral): pain starts near mouth & shoots to eye, ear, nostril on ipsilateral side
Trigeminal Neuralgia
First line tx for trigeminal neuralgia
Carbamazepine
If this is present in younger pts, suspect Multiple sclerosis
Trigeminal Neuralgia
MC type of stroke=
Ischemic
Transient episode of neurological deficits caused by focal brain, spinal cord or retinal ischemia (WITHOUT acute infarction); MC due to embolus
Transient ischemic attack (TIA)
Internal carotid artery: Amaurosis fugax (monocular vision loss-temporary “lamp shade down on one eye”), weakness in contralateral hand; sudden HA, speech changes, confusion
TIA
Mild traumatic brain injury; alteration in mental status with or loss of consciousness; confusion, amnesia, HA, dizziness, visual disturbances, delayed responses and emotional changes; signs of increased intracranial pressure (persistent vomiting, worsening HA, increasing disorientation, changing levels of consciousness)
Concussion syndrome
MC type of stroke; Most d/t thrombus (49%) others d/t embolus
Ischemic
Type of ischemia stroke; small vessel disease (penetrating branches of cerebral arteries in pons, basal ganglia); MC is hemiparesis, hemiplegia; Ataxic hemiparesis weakness/clumsiness in LEG>arm; ;dysarthria (clumsy hand syndrome); hx of HTN (80%)
Lacunar infarcts
On CT scan, small punched out hypotedense* area
Lacunar infarcts
