Term
| planning, consequences of action |
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Definition
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Definition
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| perception/recognition of stimuli, orientation and movement |
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| hearing, complex visual images, memory, perception/recognition of auditory stimuli and speech |
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| relays audio/visual info, eye movement |
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Term
| regulates vital body function: heart rate, breathing, autonomic functions |
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Definition
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Term
| relay station between medulla and cerebrum (motor/sensory info), regulates breathing |
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Definition
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Term
| balance and coordination, seat of motor control |
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Definition
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Term
| functions in higher brain processes such as thought and action. controls all voluntary activity with the help of the cerebellum |
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Definition
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Term
| bundle of axons that connect the 2 hemispheres |
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Definition
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Term
| voluntary motor movement, coordination, cognition and emotion |
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Definition
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Term
| includes the thalamus, hypothalamus, amygdala and hippocampus |
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Definition
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Term
| located in the temporal lobe, involved in memory, emotion and fear |
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Definition
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Term
| learning, memory, converts short-term memory into long-term memory |
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Definition
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Term
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Definition
| thalamus and hypothalamus |
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Term
| located deep in the forebrain, processes nearly all sensory and motor information. relays info to and from the overlying cortex- last relay site to all sensory input (except olfaction) before the information about sensory input reaches the cortex |
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Definition
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Definition
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| controls vital life functions |
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Definition
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Term
| controls eye movement, relays visual and auditiory info |
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Definition
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Term
| regulates breathing, serves as a relay station between the cerebral hemisphere and the medulla. involved in motor control and sensory inpus |
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Definition
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Term
| extension of spinal cord (located between the pons and spinal cord). regulates vital body functions (along w the pons) such as heart rate, breathing, autonomic centers, swallowing and coughing |
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Definition
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Term
| located posterior to the medulla. maintains posture and balance, coordinates voluntary movement and controls certain head and eye movements |
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Definition
| since the basal ganglia is involved in coordinated movement, emotion and cognition, problems can lead to movement disorders (dyskinesias, dystonias, parkinsonism, huntington's disease) or behavior control (tourette's, obsessive compulsive) |
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Term
| involuntary spasms, repetitive motions or abnormal voluntary movement |
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Definition
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Term
| sustained contraction (muscle spasm) especially of antagonistic muscles (ex simulatneous biceps and triceps contraction) -> twisting of the body, abnormal posturing (ex torticollis, writer's cramp) |
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Definition
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Term
| sudden brief, sporadic involuntary jerking/twitching of 1 muscle or muscle group (not suppressible) |
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Definition
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Term
| sudden, repetitive nonrhythmic movements or vocals using specific muscle groups. tics are suppressible (uinlike myoclonus which is not suppressible) ex tourette syndrome |
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Definition
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Term
| rapid involuntary jerky, uncontrolled, purposeless movements. ex huntington chorea (due to caudate nucleus atrophy in the basal ganglia), sydenham's chorea (rheumatic fever) |
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Definition
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Term
| prolonged sustained contraction/rigidiy muscle contractions |
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Definition
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Term
| repetitive rapid movement muscle contractions |
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Definition
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Term
| tremor at rest (ex parkinson disease) |
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Definition
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Term
| tremor occurs while holding position against gravity |
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Definition
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Term
| tremor occurs during movement or when approaching nearer to a target |
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Definition
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Term
| disorders associated w tremor, bradykinesia, rigidity and postural instability |
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Definition
| parkinsonism, includes parkinson disease, dopamine antagonists, lewy body disease |
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Term
| loss of the dopamine producing cells of the substantia nigra (in the basal ganglia) |
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Definition
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Term
| medications that block dopamine |
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Definition
| dopamine antagonists- typical antipsychotics, atypical antipsychotics, antiemetics |
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Term
| loss of dopaminergic neurons leads to motor features similar to parkinson disease. loss of anticholinergic neurons lead to dementia (similar to alzheimer's), visualspatial dystunctions and recurrent visual hallucinations |
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Definition
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Term
| autosomal dominant neurodegenerative disorder. mutation on chromosome 4. neurotoxicity as well as cerebral, putamen and caudate nucleus atrophy. symptoms usually appear 30-50 y of age. behavioral changes then chorea and dementia.personality, cognitive, intellectual and psychiatric changes including irritability. chorea- rapid, involuntary or arrhythmic movement of the face neck trunk and limbs initially, chorea worsened w voluntary movements and stress, usually disappears w sleep. dementia mostly before 50y (primarily executive dysfunction), gait abnormalities/ataxia (often irregular and unsteady). incontinence, facial grimacing. PE: restlessness, fragility. quick, involuntary hand movements. brisk deep tendon reflexes. CT scan: cerebral and caudate nucleus atrophy. mri shows similar findings. genetic testing. PET scan: decreased flucose metabolism in the caudate nucleus and putamen. no cure. usually fatal within 15-20 years after presentation (due to disease progression). chorea management w antidopaminergics: typical and atypical antipsychotics, Tetrabenzine, Benzodiazepines may help w chorea and sleep. no medication stops disease progression |
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Definition
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Term
| autosomal dominant inherited disorder of unknown etiology. onset of age is usually in the 60s but may occur at any age. intentional tremor- postural, bilateral action tremor of the hands, forearms, head, neck or voice. MC in the upper extremities and head (titubation) - usually spares the legs. worsened with emotional stress and intentional movement. on finger to nose testing, tremor increases as the target is approached. tremor shortly relieved with ETOH ingestion. No abnormal physical exam findings, no other significant neurologic findings besides the tremor (patient +/- cogwheel phenomenon). propanolol may help is severe or situational. primidone (barbiturate) if no relief with propanolol, instead of propranolol or with it. alprazolam (benzodiazepine) 3rd line |
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Definition
| essential familiar tremor (benign) |
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Term
| idiopathic dopamine depletion -> failure to inhibit acetylcholine in the basal ganglia (Ach is an excitatory CNS neurotransmitter, dopamine is inhibitory). onset of symptoms 45-65y MC. cytoplasmic inclusions (Lewy bodies), loss of pigment cells seen in the substantia nigra. Tremor often 1st symptom. resting tremor MC sign- pill rolling- worse at rest and w emotional stress, lessened with voluntary activity, intentional movement and sleep. usually confined to one limb or one side for years before it becomes generalized. bradykinesia: slowness of voluntary movement and dec automatic movements ex lack of swinging of the arms while walking and shuffling gait. rigidity: increased resistance to passive movement (cogwheel, flexed posture) festination = increasing speed while walking. normal deep tendon reflexes. usually no muscle weakness. face involvement: relatively immovile face (fixed facial expressions), widened palpebral fissure, Myerson's sign: tapping the bridge of nose repetitively causes a sustained blink. decreased blinking. seborrhea of the skin common. instability: postural instability usually a late finding- pull test- stand behind patient and pull shoulders -> patient falls or takes steps backwards. dementia in 50% (usually a late finding) |
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Definition
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Term
| parkinson disease management |
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Definition
1. Levodopa/Carbidopa (Sinemet): most effective treatment. Levodopa is converted to dopamine (carbidopa reduces amount of levodopa needed, reducing S/E of Levodopa). S/E: nausea, vomiting, hypotension, somnolence dyskinesia and "wearing off bradykinesia" associated with long-term use
2. dopamine agonists: bromocriptine, pramipexole, ropinirole. MOA: directly stimulates dopamine reeptors. Less S/E than Levodopa. Sometimes used in young patients to delay the use of Levodopa. If pt is not sensitive to Levodopa, they may develop an insensitivity to dopamine agonists S/E orthostatic hypotension, nausea, headache, dizziness, sleep disturbances, anorexia
3. Anticholinergics: Trihexyphenidyl, Benztropine (Cogentin). MOA: blocks excitatory cholinergic effects. Ind <70y with tremor predominance (doesn't improve bradykineasia) S/E: constipation, dry mouth, blurred vision, tachycardia, urinary retantion. CI: BPH, glaucoma
4. Amantadine- inc's presynaptic dopamine release and improves long-term levodopa induced dyskinesias. may help early on with mild symptoms
5. MAO-B inhibitors ex Selegiline, Rasagiline. MOA- increases dopamine in the striatum (MAO-B normally breaks down dopamine)
6. Catechol-O-Methyltransferase (COMT) inhibitors: Entacapone, Tolcapone. Adjunctive tx. MOA: prevents dopamine breakdown. Ex S/E GI sx, brown discoloration of urine |
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Term
| onset usually 2-5y MC in boys, may be associated w obessions-compulsions. get motor tics of face, head and neck. get verbal or phonetic ticks like grunts, throat clearing, obscene words- coprolalia, repetitive phrases, repeating phrases- echolalia. self-mutilating tics like hair pullingm nail biting. manage w habit reversal therapy, dopamine blocking agents (halperidol, risperidone, fluphenazine, pimozide, tetrabenzine), alpha-adrenergics (cliniding, guanfacine, clonazepam may be used as adjunct) |
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Definition
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Term
| necrosis of both upper and lower mnotor neurons -> progressive motor degeneration. get muscle weakness, loss of ability to initiate and control motor movements. mixed upper motor and lower motor neuron signs. bulbar symptoms: dysphagia, dysarthria, speech problems, eventual respiratory dysfunction. sensation, urinary sphincter and voluntary eye movement spared. manage w riluzole to reduce progression for up to 6 months. usually fatal within 3-5 years after onset |
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Definition
| amyotrophic lateral sclerosis (ALS), Lou gehrig's disease |
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Term
| CNS disorder associated with muscle tone and postural abnormalities due to brain injury during perinatal or prenatal period. hallmark is spasticity. varying degrees of motor deficits. often associated w intellectual/learning disabilities and development abnormalities. may develop seizures. PE: hyperreflexia, limb-length discrepancies, congenital defects. management: multidisciplinary approach, improving spacticity: Baclofen, Diazepam. antiepileptics for seizures |
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Definition
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Term
| sleep-related movement disorder. usually primary but may occur secondary to CNS iron deficiency, pregnancy, peripheral neuropathy etc. get uncomfortable or unpleasant sensation (itching, burning, paresthesias etc) in the leg that creates an urge to move the legs. symptoms: worsen at night and tend to occur w prolonged periods of rest or inactivity. during sleep, periodic limb movements may disturb sleep or cause the pt to awake from sleep. improves w movement. manage w dopamine agonists (tx of choice): pramipexole, ropinirole or alpha-2-delta calcium channel ligands like gabapentin. iron supplementation recommended in pts w serum ferritin lvls lower than 75. benzos can be used as adjunctive treatment |
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Definition
| restless legs syndrome (willis-ekbom disease) |
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Term
| acute/subacute acquired inflammatory demyelinating polyradiculopathy of the peripheral nerves. inc incidence w campylobacter jejuni (MC) or other antecedent respiratory or GI infections (CMV, EBV, HIV, mycoplasma), immunizations, postsurgical. pathophys: immune-mediated demyelination and axonal degeneration slows nerve impulses -> symmetric weakness and paresthesias. post-infection immune response cross-reacts w peripheral nerve components (molecular mimicry). get ascending weakness and paresthesias (usually symmetric) dec DTR (LMN lesion) may involve the muscles of respiration or the bulbar muscles (swallowing abnormalities) CN VII palsy. autonomic dysfunction: tachycardia, hypotension, hypertension, breathing difficulties. diagnosis: CSF shows high protein w a normal WBC count, this is known as albuminocytological dissociation, protein >400mg/L usually seen after 1-3 weeks of symptom onset. electrophysiologic studies: decreased motor nerve conduction velocities and amplitude. management: plasmapheresis best if done early. MOA removes harmful circulating auto-antibodies that cause demyelinaton. equally as effective as IVIG. pts usually hospitalized. intravenous immune globin suppresses harmful inflammatin/auto-antibodies adn induces remyelination. most recover within months. mechanical ventilation if respiratory failure develops. prednisone contraindicated. prognosis: 60% full recovery in 1 year, 10-20% left w permanent disability |
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Definition
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Term
| autoimmune peripheral nerve disorder MC in young women, associated w HLA-DR3. 75% have thymic abnormality (hyperplasia or thymoma) or other autoimmune disorders. may occur postpartum. pathophys: inefficient skeletal muscle neuromuscular transmission due to autoimmune antibodies against acetylcholine (nicotinic) postsynaptic receptor at the neuromuscular junction (decx ACh receptors) -> progressive weakness w repeated muscle use and recovery after periods of rest. ocular weakness: extraocular involvement -> diplopia, eyelid weakness/ptosis (more prominent w upward gaze). weakness worsened w repeated use. pupils are spared. generatlized muscle weakenss: least in the morning worseneed w repeated muscle use throughout the day (relieved w rest). normal sensation/deep tendon reflexes. Bulbar (oropharyngeal weakness) with prolonged chwing, dysphagia. respiratory muscle weakness may lead to respiratory failure/crisis. diagnosis w pos acetylcholine receptor antibodies, pos MuSK/ muscle-specific tyrosine kinase antibodies. Edrophoniumn (tensilon) test- rapid response to short-active IV Edrophonium in limb. CT scan or MRI of the chest may show thymoma or thyymus gland abnormality. Ice pack test- place ice on eyelid for 10 min -> improvement of ptosis in ocular |
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Definition
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Term
| Myasthenia Gravis manageemnt |
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Definition
1.acetylchlinesterase inhibitors: Pyridostigmine or Neostigmine 1st line manageemnt. short acting Edrophonium only used for diagnostic purposes. MOA: increases acetylcholine by decreasing acetylcholine breakdown. SE: abdominal cramps/diarrhea, cholinergic crisis
2.immunosuppression- plasmapheresis or IVIG used in crisis for rapid response. chronic- corticosteroids. alternatives- Azathioprine or cyclosporin
3.thymectomy if thymoma +/- helpful if not due to thymnoma
4.avoid fluoroquinolones and aminoglycosides (may exacerbate) |
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Term
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Definition
| excess acetylcholine due to Ach-esterase inhibition -> weakness, nausea, vomiting, pallor, sweating, salivation, darrhea, miosis, bradycardia, respiratory failure. in myasthenia gravis, it can be difficult to determine if the weakness and respiratory failure is from myasthenic crisis (severe manifestation of myasthenia gravis) or cholinergic crisis (result of too much acetylcholine from acetylcholinesterase inhibitors). if flaccid paralysis improves w Tensilon -> myasthenic crisis. If flaccid paralycis worsens w tensilon -> cholinergic crisis |
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Term
| MC associated w small cell lung cancer. Antibodies against presynaptic voltage-gated calcium channels prevents acetylcholine release. unlike myasthenia gravis, weakness improves w repeated use |
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Definition
| myasthenic syndrome (lambert-eaton) |
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Term
autoimmune, inflammatory demyelinating disease of the CNS of idiopathic origin. associated w axon degeneration of white matter of the brain, optic nerve and spinal cort. MC in women and young adults 20-40y. Associated w CNS IgG production and T-cell reaction. Relapsing-remitting disease MC: episodic exacerbations. Progressive disease: progressive decline without acute exacerbations. Secondary progressive: relapsing-remitting pattern that becomes progressive.
1. sensory deficits- pain, fatigue (75%), numbness, paresthesias in the limbs, muscle cramping. trigeminal neuralgia, Uhthoff's phenomenon: worsening of symptoms w heat (ex exercise, fever ,hot tubs), Lhermitte's sign: neck flexion causes lightning-shock type pain radiating from the spine down the leg
2. optic neuritis (retrobulbar): unilateral eye pain worse w eye movements, dipolopia, central scotomas, vision loss (esp color). marcus-Gunn pupil: during swinging-flashlight test from the unaffected eye into the affected eye, the pupils appear to dilate (due to less than normal pupillary constriction) This response is due to the brain perceiving the delayed conduction of affected optic nerve as if light was reduced.
3. Motor: upper motor neuron involvement = spasticity and positive (upwards) Babinski.
4.Spinal cord symptoms: bladder, bowel, or sexual dysfunction.
5. charcot's neurologic triad 1. nystagmus 2. staccato speech and 3. intentional tremor. |
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Definition
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Term
| MS diagnosis and manageemnt |
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Definition
-at least 2 discrete episodes of exacerbations
-MRI with gadolinium: white matter plaques (hyperdensities)w . high intensity is hallmark finding. there should be proof at least 2 areas of white matter involvement before the diagnosis is made
2. lumbar puncture: inc IgG oligoclonal bands in CSF: small discrete bands in teh gamma globulin region seen on electrophoresis which reflects inflammatory cells penetrating the blood brain barrier.
-treat acute exacerbations w IV corticosteroids (high-dose) 1st line. Immunomodulators ex Cyclophosphamide. Plasmapheresis if not responsive to corticosteroids
-relapse-remitting/progressive disease treat w B-interferon or Glatiramer acetate (Copaxone) decrease #/severity of relapses
-amantadine is helpful for fatigue
-Baclofena nd Diazepam for spasticity |
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Term
idiopathic, unilaterial CN VII/facial nerve palsi-> hemifacial weakness/paralysis due to inflammation or compression. lower motor lesion. strong association w herpes simplex virus reactivation. MC on the right side (60%)
risk factors: diabetes mellitus, pregnancy esp 3rd trimerster, post URI, dental nerve block
-get sudden onset of ipsilateral hyperacusis (ear pain) 24-48 hours -> unilateral facial paralysis: unable to lift affected eyebrow, wrinkle forehead, smile on affected side, loss of the nasolabial fold, drooping of the corner of mouth, taste disturbance (anterior 2/3), biting innercheek, eye irritation (due to decreased lacrimation and inability to fully close eyelid. bell phenomenon: eye on the affected side moves laterally and superiorly when eye closure is attempted. weakness/paralysis only affects the face (not extremities)
-diagnosis of exclusion
-no treatment is required, nmost cases resolve w/i 1 month. can use prednisone to dec nerve inflammation if started within 1st 72 hr of sx onset. artificial teart to reduce vision problems +/- eye patch. +/- acyclovir in severe cases
-function of ten begins to return within 2 weeks w significant improvements w/i 4 months w or w/o treatment
-restoration of taste usually rpecedes motor recovery |
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Definition
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Term
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Definition
| 90% migraine, tension,cluster or rebound. primary = idiopathic in nature. tension and migraine MC in women |
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Term
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Definition
| 4% meningitis, subarachnoid hemnorrhage, intracranial hypertension, hypertensive crisis, acute glaucoma, suspect 2rd if abrupt or progression of severity |
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Term
| MC overall type of headache. mean age of onset ~30y. thought to be due to mental stress. bilateral, tight, band-like, vise-like constant daily headache. worsened w stress, fatigue, noise or glare (not worsened w activity like w migraines) usually not pulsatile. no neausea, vomiting or focal neurologic symptoms (ex no photophobia or phonophobia). treated like migraines- 1st line SNAIDs, aspirin, acetaminophen. anti-migraine medications. TCAs (ex Amitriptyline) in severe or recurrent cases, prophylaxis. beta-blockers. psychotherapy |
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Definition
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Term
MC in women. 2 types: w/o aura (common) and rarer w/ aura 9classic). MC cause of morning headache. family history 80%. thought to be caused by vasodilation of the blood vessels innervated by the trigeminal nerve. neruological findings thought to be due to internal carotid artery constriction
-lateralized, pulsatile/throbbing headache assocaited w nausea/vomiting, photophobia and phonophobia usually 4-72 hrs in duration. may be bilateral. worse w physical activity, stress, lack/excessive sleep, ETOH, specific foods (ex chocolate, red wine), OCPs/menstruation
-auras: visual changes MC. ex light flashes (photopsia), zig zag lines of light (teichopsia), scotomas (blind spots that may scintillate), aphasia (impairment of language), weakness, numbness, auras usually last <60 minutes (5-20 minutes common) -> headache onset |
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Definition
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Term
| migraine headache management |
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Definition
1. symptomatic (abortive):
-triptans or ergotamines MOA: serotonin 5HT-1 agonists -> vasoconstriction. S/E : chest tightness from constriction, nausea, vomiting, abdominal cramps. CI: coronary artery or peripheral vascular disease, uncontrolled HTN (due to vasoconstriction), hepatic or renal disease, pregnancy
-Dopamine blockers: IV phenothiazines: Metoclopramide, Promethazine, Prochlorperazine, Ind: antiemetics for nausea and vomiting. given w diphenhydramine (benadryl) to prevent EPS, dystonic reactions and parkinsonism symptoms due to decreased dopamine
-Iv fluids and placing the pt in dark, quiet room helps most suffering an acute attack
-mild symptoms: NSAIDs/acetaminophen 1st line. codeine or barbiturates may be used. some migraine medications have caffeine added to it to improve symptoms
2. prophylactic: Anti-HTN meds: B-blockers, calcium channel blockers. tricyclic antidepressants. anticonvulsants (valproate, topiramate), NSAIDs |
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Term
| pathophys: compression of the trigeminal nerve root (by superior cerebellar artery or vein) 90%. idiopathic 10%. MC in mid-aged women. clinical manifestations- brief, episodic, stabbing/lancinating pain in the 2nd/3rd division of Trigeminal nerve CN V lasting seconds-min worse w touch, eating, drafts of wind and movements (often unilateral). pain starts near mouth and shoots to the eye, ear and nostril on the ipsilateral side. management: carbamazeping 1st line. oxcarbazepine. MOA unknons S/E drowsiness, nausea, vomiting, leukopenia. gabapentin (neurontin), baclofen, suspect multiple sclerosis in younger pts with this. surgical decompression may be used in severe or recalcitrant cases |
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Definition
| trigeminal neuralgia (TGN) (Tic douloureux) |
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Term
predominantly young and middle-aged males. severe unilateral periorbital/temporal pain (sharp, lancinating) bouts lasting <2 hours with spontaneous remission. bouts occur several times a day over 6-8 weeks. triggers: worse at night, ETOH, stress or ingestion of specific foods
PE: ipsilateral horner's syndrome (ptosis, miosis, anhydrosis), nasal congestion/rhinorrhea, conjunctivitis and lacrimation
management: 100% oxygen 1st line 6-10L, anti-migraine meds help during attack: SQ sumatriptan or ergotamines (vasoconstriction). prophylaxis w verapamil 1st line, corticosteroids, ergotamines, valproic acid, lithium, cyproheptadine |
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Definition
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Term
| idiopathic w no other cause evident, MC in obese women of childbearing age. can be caused by corticosteroid withdrawal, growth hormone, thyroid replacement ,OCPs. systemic diseases may also be causative in susceptible patients. headache worse w straining, retrobulbar pain, nausea, vomiting, tinnitus, visual changes (may lead to blindness if not treated). funduscopic exam: papilledema, may have visual field loss. +/- CN6 palsy = lateral rectus muscle weakness -> limitation of abduction (induces estropia/turning inward towards the nose) esp looking in the distance. CT scan 1st to rule out CNS mass -> lumbar puncture: increased CSF pressure otherwise normal. manage w acetazolamide (reduces CSF pressure/production) +/- furosemide +/- short-course of steroids. optic nerve sehath fenestration or CSF shunting allows evacuation of CSF, improving vision |
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Definition
| idiopathic intracranial HTN (pseudotumor cerebri) |
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Term
| high IgG(oligloclonal bands) in csf |
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Definition
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Term
| high protein w normal WBC/cell count in csf |
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Definition
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Term
| high protein w inc WBC (primarily polymorphonuclear neutrophils), dec glucose in CSF |
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Definition
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Term
| normal glucose, inc WBCs (lymphs) in CSF |
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Definition
| viral (aseptic) meningitis |
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Term
| dec glucose, inc WBCs (lymphs) in CSF |
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Definition
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Term
| inc CSF pressure otherwise normal |
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Definition
| inc idiopathic intracranial htn |
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Term
| xanthocromia, blood in CSF |
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Definition
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Term
dilation of the cerebral ventricles w normal opening pressures on lumbar puncture. unknown cause but thought o be due to impaired CSF absorpiton after a CNS injury (ex subarachnoid hemorrhage, tumors, CNS infection, inflammatory disease, head injury etc)
classic tirad: dementia, gait disturbance and urinary incontinence
gait disturbances: wide-based, shuffling giat - described as gait apraxia or "magnetic" gait (as if the feet are stuck to the floor). may be associated w postural instability. dementia: includes impaired executive function, psychomotor depression, apathy. urinary incontinence: may present as urinary urgency early in the disease. other: weakness, lethargy, malaise, rigidity, hyperreflexia and spasticity. diagnosis: MRI or CT scan: enlarged ventricles in the absence of or out of proportion to sulcal dilation. MRI superior. LP: CSF pressure is usually normal. lumbar tap test = removal of up to 50cc of CSF leads to improvement of symptoms 30-60 minutes after the procedure. management: ventriculoperitoneal shunt tx of choice. gait abnormalities usually the most improved |
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Definition
| normal pressure hydrocephalus |
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Term
mild traumatic brain injury -> alteration in mental status with or without loss of consciousness. confusion: confused or blank expression, blunted affect. amnesia: pretraumatic (retrograde) or prosttraumatic (antegrade) amnesia. the duration of retrograde amnesia is usually brief. headache, dizziness, visual disturbances: blurred or double vision. delayed responses and emotional changes: emotional instability. signs of inc intracranial pressure: persistent vomiting, worsening headache, increasing disorientation, changing levels of consciousness
diagnosis: CT scan: study of choice for evaluating acute head injuries. MRI: study of choice if prolonged symptoms >7-13 days or w worsening of symptoms not explained by concussion syndrome. PET scan may be done to look at glucose uptake (not done often). management: cognitive and physical rest is the main management. pts may resume strenuous activity after resolution of symptoms and recovery of memory and cognitive functions |
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Definition
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Term
| acute, abrupt transient confused state due to an identifiable cause (ex medications, infections, etc). rapid onset associated with fluctuating mental status changes adn marked deficit in short-term memory. usually associated with full recovery within 1 week in most cases |
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Definition
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Term
| progressive, chronic intellectual deterioration of selective functions: memory loss and loss of impulse control, motor and cognitive functions. includes language dysfunctions, disorientation, inability to perform complex motor activities and inappropriate social interaction. not due to delirium, mnedications or psychiatric illness. risk factors: age (esp >60y) and vascular disease |
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Definition
| dementia (includes alzheimer's disease, vascular, frontotemporal, diffuse lewy body, crutzfeld-jakob) |
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Term
| 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, normal reflexes. short-term memory loss 1st symptom, progresses to long-term memory loss, disorientation, behavioral and personality changes. usually gradual in nature. diagnosis: CT scan: cerebral cortex atrophy on CT scan, may be used to rule out other causes as well. management: Ach-esterase inhibitors: Donepezil (Aricept), Tacrine, Rivastigmine, Galantamine MOA: reverses cholinergic deficiency and symptom relief (does not slow down disease progression). NMDA antagonist: Memantine MOA: blocks NMDA receptor, slowing calcium influx and nerve damage. glutamate is an excitatory neurotransmitter of the NDMA receptor. excitotoxicity causes cell death. NMDA antagonists reduce glutamate excitotoxicity. may be adjunctive |
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Definition
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Term
| 2nd jMC type. brain disease due to chronic ischemia and multiple infarctions (ex lacunar infarcts). hypertension most impt risk factor. HTN control may slow disease progression. clinical manifestations: Cortical: forgetfulness, confusion, amnesia, executive difficulties, speech abnormalities. Subcortical: motor deficits, gait abnormalities, urinary difficulties, personality changes |
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Definition
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Term
| rare type. localized brain degeneration of the frontotemporal lobes. may progress globally. marked personality changes (preserved visuospatial), aphasia. behavioral symptoms: apathy, disinhibition. pos palmomental and palmar grasp reflexes. usually no amnesia present. pos pick bodies |
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Definition
| frontotemporal demenita (pick's disease) |
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Term
| Lewy bodies: abnormal neuronal protein deposits. diffuse in comparison to (parkinson disease - localized). visual hallucinations, delusions, episodic delirium, parkinsonism. dementia occurs later in the disease |
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Definition
| diffuse lewy body disease |
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Term
| upper motor neuron lesions |
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Definition
| connects to LMN in spinal cord. neurotransmitter glutamate transmits nerve impulses form upper motor to lower motor neurons via glutamate receptors on the receiving LMN. Etiologies: Stroke/CVA, Multiple sclerosis, Cerebral palsy, Brain or spinal cord damage (ex traumatic brain injury). Spastic paralysis (hypertonia) with inc DTR (due to removal of inhibitory influence of the cortex), weakness. no fasciculations. upward babinski reflex (abnormal >2y), little or no muscle atrophy |
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Term
| lower motor neuron lesions |
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Definition
| LMN are located in the spinal cord and links the UMN to the muscles. LMN stimulated by glutamate release from UMN causing depolarizaiton of LMN. LMN terminates at the effector (muscle) at the neuromuscular joint. Acetylcholine release by the LMN stimulates muscle contraction at the neuromuscular joint. Etiologies: guillain-barre syndrome, botulism, poliomylitis, cauda equina syndrome, bell palsy. flaccid parlysis (loss of muscle tone/hypotonia) dec DTR, weakness. fasciculations (end stage muscle xcenervation), downward babinski reflex. muscle atrophy (neurogenic degeneration) |
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Term
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Definition
Eye opening. spontaneous- 4 response to verbal commands- 3 response to pain- 2 no eye opening- 1
best verbal response: oriented- 5 confused- 4 inappropriate words- 3 no verbal response- 1
Best motor Response: obeys commands- 6 localizing response to pain- 5 withdrawal response to pain- 4 flexion to pain- 3 extension to pain-2 no motor response- 1
mild brain injury >/= 13, 9-12 moderate, |
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Term
| derived from star-shaped glial cells of the brain and spinal cord that support the endothelial cells of the blood-brain barrier, provide nutrients for cells, maintain extracellular ion balance and also repair the brain after injury. can appear in any part of the brain. most often infratentorial in children (supratentorial in adults). focal deficits MC. depends on teh location of the lesion. MC in frontal and temporal areas of the cerebral hemisphere. general sx: headaches (may be worse in the morning, may wake pts up at night, may be positional), cranial nerve deficits, altered mental status changes, neurological deficits, ataxia, vision changes, weakness. Increased intracranial pressure: due to mass effect -> headache, nausea, vomiting, papilledema, ataxia, drowsiness, stupor. diagnosis: CT scan or MRI w contrast. brain biopsy. Management: surgical excision or chemotherapy or radiation |
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Definition
astrocytoma
pilocytic astrocytoma (grade I) (juvenile astrocytome) - typically localized. considered the "most benign" (noncancerous) of all the astrocytomas. MC in children and young adults. other grade I astrocytomas include cerebellar astrocytoma and desmoplastic infantile. diffuse astrocytoma (grade II or low-grade) types: fibrillary, gemistocytic and protoplasmic. they tend to invade surrounding tissues but grow at a relatively slow pace. Anaplastic astrocytoma (grade III) rare but aggressive. grade IV astrocytoma (glioblastoma multiforme)- MC primary CNS tumors in adults. Subependymal giant cell astrocytoma- ventricular tumors associated with tuberculous sclersosis |
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Term
| MC and most aggressive of all the primary CNS tumor in adults (>50%). Primary: MC (60%). seen in adults >50y. Arises de novo (new). MC type and most aggressive. secondary: 40%, MC <45y. due to malignant progression, may transform as early as 1 year or >10y. risk factors: males >50y, HHV-6 and cytomegalovirus infections, ionizing radiation. classic type: 97%, presence of extra copeis of epidermal growth factor receptor gene (EGFR) TP53 rarely mutated in this type (note that the others are associated with TP53 mutation). Mesenchymal: high rates of mutations and alterations including the gene encoding for neurofibromatosis type 1. TP53 often mutated. an alteration of MGMT (a DNA repair enzyme). clinical manifestations: 1. focal deficits MC. depends on the location of the tumor. MC in frontal and temporal areas of the cerebral hemisphere. general: headaches (may be worse in the morning, may wake patients up at night, may be positional), cranial nerve deficits (ex fixed, dilated pupil from a CN III palsy), altered mental status, neurological deficits, ataxia, vision changes, weakness. frontal lobe: dementia, personality changes, gait abnormalities, expressive aphasia, seizures. tesmporal lobe: partial complex and generalized seizures. parietal lobe: receptive aphasia, contralateral sensory loss, hemianopia, spatial disorientation. occipital lobe: contralateral homonymous hemianopia. thalamus: contralateral sensory loss. brainstem: papillary changes, nystagmus, hemiparesis. 2. increased intracranial pressure: due to mass effect -> headache, nausea, vomiting, papilledema, atazia, drowsiness, stupor. Cushing's reflex: in severe cases: triad 1- irregular respirations 2- hypertension and 3- bradycardia. diagnosis w 1. CT scan or MRI w contrast: tumor has a variety of appearances on imaging (depending on the amount of hemorrhage, necrosis or its age). MC seen in the subcortical white matter of the cerebral hemispheres. -nonhomogenous mass w a hypodense center and a variable ring of enhancement surrounded by edema. mass effect may cause hydrocephalus -may cross the corpus callosum (butterfly) 2. brain biopsy- histologic appearance: presence of small areas of necrotizing tissue (from myelin breakdown) surrounded by anaplastic cells and hyperpalstic blood vessels with areas of hemorrhage. cells may have stem-cell like properties. pseudopalisading: tumor cells lining the area of necrosis. management: surgical excision, radiotherapy and adjuvant chemotherapy with Temozolomide (alkylating agent), poor prognistis (often <1 year surival) |
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Definition
Glioblastome (Glioblastoma Multiforme)
Glioblastoma = Grade IV astrocytoma: heterogenous mixture of poorly differentiated astrocytes. |
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Term
| usually benign tumor arising from meningiothelial arachnoid cells of the meninges (covering the brain and spinal cord). Normally these cells provide a barrier function of the CNS system as part of the meninges, help to clear waste products from the CSF and helps to maintain optic nerve microenvironment. 2nd MC primary CNS neoplasm. MC in women (associated w neurofibromatosis- esp NF-2), MC arise from dura or sites of dural reflection (ex venous sinuses, falx cerebri). most are asymptomatic. often found incidentally on imaging for other reasons. focal deficits: includes seizures, progressive spasticity, weakness or other motor/sensory symptoms. symptoms due to increased intracranial pressure not as common. focal deficits: includes seizures, progressive spasticity, weakness or other motor/sensory symptoms. symptoms due to increased intracranial pressure not as common. diagnosis w CT scan or MRI w contrast- see intensely enhancing, well-defined lesion often attached to the dura. histologic appearance of brain biopsy: spindle-cells concentrically arranged in a whorled pattern. psammoma bodies: concentric round calcifications. management- asymptomatic- observation. symptomatic- surgical removal |
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Definition
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Term
-primary- seen w/o evidence of systemic disease. variant of extranodal NHL. 2ry more common.
-secondary- METS from another site (ex NHL in the neck, chest, groin, abdomen) esp diffuse large B cell lymphoma (90%), Burkitt's lymphoma (10%)
-risk factors- immunosuppression, Epstein Barr virus pos in 90% of these pt
-focal deficits: MC. Depends on the location of the lesion. Ocular symptoms: visual changes, steroid-refractory posterior uveitis. Diagnosis: CT scan or MRI w contrast shows hypointense ring-enhancing lesion in deep white matter on CT. Biopsy- usually guided by imaging study. workup includes CT of abdomen/pelvis, PET scan, bone marrow biopsy, slit lamp examination. management: Chemotherapy: Methotrexate most effective chemotherapy (given w folinic acid/leucovorin). chemotherapy usually not given at same time as radiation therapy. radiation therapy, corticosteroids: partial response. surgical resection usually ineffective |
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Definition
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Term
| cell that makes up the supportive (glial) tissue of teh brain. these tumors can be found anywhere within the cerebral hemispheres (esp the frontal and temporal lobes). may be asymptomatic. may be incidental finding. focal deficits: includes seizures, headaches and personality changes, depends on the tumor location. diagnosis: CT scan or MRI w contrast. Brain biopsy: usually guided by imagin studies. histologic appearance: soft, grayish-pink calcified tumors, areas of hemorrhage and or cystic. chicken-wire capillary pattern w "fried-egg shaped" tumor cells seen w microscope. management- surgical resection standard tx +/- radiation and/or chemotherapy (ex anaplastic) |
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Definition
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Term
| MC in children. MC seen in 4th ventricle (+/- cause hydrocephalus) +/- medulla, spinal cord. cauda equina in adults. infants: inc in head size, irritability, sleeplessness and vomiting. older children/adults: nausea, vomiting, headache. diagnosis: CT scan or MRI w contrast: hypointense T1, hyperintense T2, enhances w gadolinium. brain biopsy: perivascular pseudorosettes (tumor cells surrounding a blood vessel). management: surgical resection -> adjuvant radiation therapy. chemotx not as helpful usually |
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Definition
Ependymoma
(ependymal cells line the ventricles and parts of the spinal column) |
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Term
| abnormal buildup of blood vessels in the skin or internal organs. 2% of all 1ry brain tumors. 10% have von Hippel-Lindau syndrome. diagnosis: CT scan or MRI. biopsy: well-defined borders, usually does not invade surrounding healthy tissue. foam cells w high vascularity. management: surgical resection. radiation may be used in tumors attached to the brainstem |
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Definition
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Term
| arises from the blood vessel lining. benign, slow growing well-defined tumors. MC found in the posterior fossa (brainstem and cerebellum) often >40y. may occur in the cerebral hemispheres or spinal cord. retinal associated w von Hippel-Lindau syndrome |
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Definition
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Term
| originate from the cells surrounding the blood vessels and the meninges. may spread to the lung and liver |
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Definition
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Term
-can't walk- lower extremity motor deficit
-loss of temp and pain sensation
-bladder dysfunction, lower extremity involvement
-flexion compression injuries common mechanism
-MC after blowout vertebral body burst fractures
-aortic dissection, SLE, AIDS can cause
-lower extremity motor deficit > upper (corticospinal)
-sensory deficits: pain, temp (spinothalamic tract), light touch, bladder retention, incontinence
-preserved proprioception, vibration, pressure (dorsal column spared)
-light touch preservation |
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Definition
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Term
-extension injuries (hyperextension injuries, ex 50% occur c MVA, falls in elderly, gun shot wounds, tumors, cervical spinal stenosis, syringomyelia)
-loss of pain and temp sensation (spinothalamic tract)
-upper extremity > lower extremity (esp hands and distal portion of UE- corticospinal)
-shawl distribution
-MC incomplete cord syndrome
-affects primarily the central gray matter (including the spinothalamic tracts)
-preserved proprioception, vibration, pressure (dorsal column spared) |
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Definition
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Term
motor, vibratory and proprioception deficits
-pain and temp deficits occuring usually 2 levels below the level of injury
-stabbing penetration injuries
-ipsilateral motor (lateral corticospinal tract), vibratory and proprioception deficits (dorsal column)
-contralateral pain and temp deficits (lateral spinothalamic tract, usually 2 levels below the injury where the spinothalamic tract crosses at the spinal cord level)
-unilateral hemniseciton of the spinal cord |
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Definition
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Term
rare, loss of proprioception and vibratory sense only
-preserved pain and light touch, no motor deficits |
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Definition
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Term
-left hemiparesis (weakness)
-left sensory loss, L-sided neglect, anosognia
-left homonymous hemianopsia, apraxia
-dysarthria, spatial/time deficits
-flat affect, impaired judgement, impulsivity |
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Definition
| anterior circulation ischemic stroke lesions- non dominant side lesions (usually right hemisphere) right side: behavior, learning process, short term memory) |
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Term
-right hemiparesis
-right sensory loss
-right homonymous hemianopsia
-dysarthria
-aphasia, agraphia, dec math comprehension |
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Definition
| anterior circulation ischemic stroke lesions (dominant side lesions, usually left hemnisphere, left side:speech language) |
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Term
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Definition
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Term
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Definition
| inability to articulate words |
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Term
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Definition
| loss of ability to execute purposeful movements |
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Term
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Definition
| loss of coordinated movements |
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Term
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Definition
| difficulty remembering words, speaking, writing |
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Term
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Definition
| frontal lobe nonfluency, sparse output (comprehension relativecly preserved) |
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Term
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Definition
| fluent aphasia (voluminous, meaningless) w markedly impaired comprehension |
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Term
-MC due to embolus (ex heart, carotid, vertebrobasilar) or transient hypotension
-50% of pts will have a CVA within 1st 24-48h afterwards (esp if DM, HTN). 10-20% will experience CVA within 90 days
internal carotid artery: amaurosis fugax (monocular vision loss- temporary "lamp shade down on one eye", weakness contralateral hand. ICA/MCA/ACA: cerebral hemisphere dysfunction. other sx: sudden headache, speech changes, confusion. PCA: somatosensory deficits
-vertebrobasilar: brainstem/cerebellar symptoms (ex gait and proprioception, dizziness, vertigo)
-diagnosis: CT scan of head initial test of choice to rule out intracranial hemorrhage. Carotid Doppler: Carotid endarterectomy recommended if pt has internal or common carotid artery stenosis >/= 70% (associated w 80% reduction in mortality). CT angiography, MR angiography, Transcranial Doppler- images cerebral vasculature for stenosis or occlusion. Blood glucose to ruloe out hypoglycemia, rule out electrlyte abnormalities, coagulation studies, CBC
-Echocardiogram: TTE or TEE: to look for cardioembolic sources
-ECG: to look for atrial fibrillation (A-bif can cause emboli)
-ABCD^2 score: to assess CVA risk (Age, Blood pressure, clinical features, duration of sc/diabetes mellitus)
management:
-aspirin +/- dipyridamole or clopidogrel (plavix). aspirin/dipyridamole (aggrenox). thrombolytics contraindicated!
-place in supine position to inc cerebral perfusion. avoid lowering blood pressure (unless >220/120)
-reduce modificable risk factors: 1- DM (glucose control) 2- HTN (BP control) 3- A fib (warfarin)
-transient episode of neurological deficits caused by focal brain, spinal cord or retinal ischemia w/o acute infarction, often lasting <24hr - most resolve in 30-60 min. |
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Definition
| Transient ischemic attack TIA |
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Term
-small vessel disease (penetrating branches on cerebral arteries in pons, basal ganglia) 1- pure motor MC (hemiparesis, hemiplegia) 2- ataxic hemiparesis and clumsiness leg > arm. 3- dysarthria (clumsy hand syndrome) 4- pure sensory loss (numbness, paresthesias) hx of HTN 80%.
- CT scan: small punchedout hypodense areas. lesions usually central and in concortical areas: ex basal ganglia
-management: aspirin. control risk factors (HTN, DM) good prognosis: partial or complete deficit resolution ranging from hrs up to 6 weeks |
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Definition
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Term
-contralateral sensory/motor loss/hemiparesis: greater in face, arm >leg/foot
-visual: contralateral homonymous hemanopsia- gaze preference towards side of lesion (x1-2 days)
-dominant (usually L-side): aphasia: broca (expressive), wernicke (sensory), math comprehension, agraphia
-nondominant (usually r-side): spatial deficits, dysarthria, left-side neglect, anosognia, apraxia) |
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Definition
| middle cerebral artery (MC type 70%) ischemic stroke |
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Term
-contralateral sensory/motor loss/hemiparesis: greater in leg/foot > upper extremity -> abnormal gait
-face spared: speech preservation. slow responses
-frontal lobe and mental status impairment: impaired judgement, confusion. personality changes (flat affect)
-urinary incontinence: upper motor neuron weakness
-gaze preference towards side of the lesion |
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Definition
| ischemic stroek: anterior cerebral artery (2%) |
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Term
| visual hallucinations, contralateral homonymous hemanopsia. "crossed sx" (ipsilateral cranial nerve deficits + contralateral muscle weakness), coma, drop attacks |
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Definition
| posterior cerebral artery ischemic stroke (posterior circulation) |
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Term
| cerebellar dysfunciton, CN palsias, dec vision, dec bilateral sensory |
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Definition
| basilar artery ischemic stroke (posterior circulation) |
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Term
| vertigo, nystagmus, N/V, diplopia, ipsilateral ataxia |
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Definition
| vertebral artery ischemic stroke (posterior circulation) |
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Term
-arterial bleed MC between skull and dura
-MC after Temporal bone fracture -> middle meningeal artery disruption
-clinical manifestations varies. brief LOC -> lucid interval -> coma; headache, N/V, focal neuro sx, rhinorrhea (CSF fluid)
-CN III palsy if tentorial herniation
-diagnosis: CT: convex (lens-shaped) bleed
-does not cross suture lines. usually in temporal area
-,anagement: +/- herniate if not evacuated early, observation if small. if inc ICP: mannitol, hyperventilation, head elevation, +/- shunt |
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Definition
| epidural hematoma (hemorrhage) |
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Term
-venous bleed MC, between dura & arachnoid due to tearing of cortical bridging veins, MC in elderly
-MC blunt trauma often causes bleeding on other sid eof injury "contre-coup"
-venous bleed
-clinical manifestations vary, amy have focal neuro sx
-diagnosis: CT: concave crescent-shaped bleed, bleeding can cross suture lines
-management: hematoma evacuation vs supportive evacuation if massive or >/= 5mm midline shift |
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Definition
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Term
-location: intraparenchymal. mechanism: HTN, AVM, trauma, amyloid ArterioVenous Malformatoin
-Headache, N/V +/- LOC, hemiplegia, hemiparesis, not associated w lucid intervals.
-diagnosis: CT intraparenchymal bleed. do NOT perform LP if suspected bc it may cause brain herniation
-management: supportive- gradual BP reduction. +/- Mannitol if inc ICP. +/- Hematoma evacuation if mass effect |
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Definition
| Intracerebral Hemorrhage (ICH) |
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Term
| bacterial infection of the meninges |
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Definition
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Term
| NOT cause by pyogenic bacterial. includes viral, fungal and tuberculosis |
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Definition
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Term
fever/chills (95%), meningeal sx: headache/nuchal rigidity (stiff neck), photosensitivity, nausea/vomiting -> AMS, seizures
-pos Kernig's sign: inability to straighten knee w hip flexion
-pos brudzinski's sign: neck felxion produces knee/ hip flexion
diagnosis: LP: CSF examination definitive dx: inc 100-10,000 PMN (neutrophils), dec glucose <45, inc total protein, inc CSF pressure. DO NOT wait for lumbar puncture to starte empiric antibiotics. early antibiotic thearpy has been shown to inc survival rates. Head CT scan: done to r/o mass effect BEFORE LP if high risk (>60y, immunocompromised, h/p CNS dz, AMS, focal neuro findings, papilledema
-dexamethasone is recommended if known or suspected Strep pneumoniae also in children if due to H influenze-B (reduces hearing loss). Post-exposure prophylaxis: ciprofloxacin 500mg PO x 1 dose. alternative Rifampin 600mg PO q12h x 2days |
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Definition
| acute bacterial meningitis |
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Term
| meningitis pathogens by age |
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Definition
<1 month: Group B Strep (Strep agalactiae) MC 70%, Lm onocytogenes, E. coli, S. pneumoniae. Ampicillin + Cefotaxime or Aminoglycoside (Ampicillin covers Listeria). This regimen also used if 1-3 months old
1mo-18y N. meningitidis MC (associated w petechial rash) S.pneumo, H. Influenzae- treat w Ceftriaxone (or Cefotaxime) + Vancomycin
18y-50y S. PNEUMO (50%) MC, N. MENINGITIDIS (+ ACCOMPANYING PETECHIAL RASH); H. INFLUENZAE, LISTERIA MONOCYTOGENES, GRAM NEG RODS. TREAT W Ceftriaxone (or Cefotaxime and Vancomycin).
>50y S. pneumo, Listeria monocytogenes, gram neg rids. Treat w Ampicillin and Ceftriaxone (or Cefotaxime) and Vancomycin
Dexamethasone recommended if known or suspected Strep pneumoniae |
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Term
| inc opening pressure >20. turbid bacterial meningitis, high protein >200, markedly dec glucose <40, inc WBC >100-100,000, >80% neutrophils, pos gram stain (60-90%). if wbc is predominantly neutrophils then bacterial is more likely |
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Definition
| bacterial meningitis findings |
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Term
| normal or mildly inc opening pressure, clear appearance, <100 protein, normal glucose, lymphs >10-300, neg gram stain. if glucose is normal then viral meningitis is most likely |
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Definition
| viral meningitis findings |
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Term
| variable (normal or mildly inc opening pressure), fibrin webs appearance, inc protein >58, dec glucose, inc lymphocytes, neg gram stain |
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Definition
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Term
| viral infection of the meninges. enterovirus MC cause (echovirus, coxsackie) esp summer and fall. arboviruses (arthropod borne- st. louis- dysuria and pyuria, west nile virus- severe lethargy, colorado tick fever, mumps HSV 1&2, HIV. headache, fiver mild confusion. pos meningeal sx: nuchal rigidity, pos burdzinski and kernig, photophobia, photophobia, lethargy. meningeal symptoms not as intense as seen in bacterial meningitis. associated w normal cerebral function, not commonly associated w focal neurological deficits nor seizures. CSF analysis: most impt test to differentiate. CT scan done 1st to rule out intracranial mass. lymphocytosis, normal glucose, mildly increased protein. MRI: diffuse enhancement of the meninges, frontal and temporal enhancement seen w HSV-1, serologies, viral cultures. management is supportive care: antipyretics, IV fluids, antimetics. good prognosis, usually self-limited (lasting on avg 7-10 days), inc fatality seen in neonates |
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Definition
| viral (aseptic) meningitis etiologies, clinical manifestations, diagnosis, management, prognosis |
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Term
| viral infection of the brain parenchyma, HSV-1 MC cause of encephalitis, enteroviruses (echovirus, coxsackie), arboviruses (west nile), varicella zoster, rubeola, toxoplasmosis, CMV, Rabies (Rhabdovirus), headache, fever. profound lethargy, AMS. associated with abnormal cerebral function, since brain parenchyma is affected, encephalitis associated with focal neurologic deficits: ex cranial nerve deficits (esp CN II, IV, VI, VII), sensory and motor deficits, personality, movement, speech and behavioral disorders, seizures. CSF analysis same as viral (aseptic) meningitis, lymphocytosis, normal glucose, inc protein. brain imaging: temporal lobe MC involved (may show mass effect). supportive care: antipyretics, IV fluids, control cerebral edema, seizure prophylaxis if needed, protect the airway if needed. Valacyclovir if HSV or no identifiable cause of meningitis (HSV associated w poor prognosis) +/- immunoglobulin if immunocompromises. associated w higher morbidity and mortality than viral meningitis. HSV encephalitis associated with up to 70% mortality if not treated |
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Definition
| encephalitis etiologies, clinical manifestations, diagnosis, management, prognosis |
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Term
| encephalitis vs meningitis |
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Definition
| encephalitis associated w abnormal cerebral function (sensory/motor deficits, speech/movement disorders). HSV-1 MC cause. meningitis not usually associated with abnormal cerebral function. Echovirus family MC cause |
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Term
| consciousness fully maintained. EEG shows focal discharge at the onset of seizures. may have focal sensory, autonomic, motor sx, may be followed by transient neurologic deifcit (Todd's paralysis) lasting up to 24 hrs. |
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Definition
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Term
| consciousness impaired, starts focally, EEG: interictal spikes with slow waves in the temporal area. aura (seconds - minutes) -> impaired consiousness |
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Definition
| complex partial (temporal lobe) seizures |
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Term
| sensory/autonomic/motor symptoms of which the patient is aware of. may precede/accompany or follow a seizure |
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Definition
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Term
| lip smacking, manual picking, patting, coordinated motor movement (ex walking) |
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Definition
| automatisms. (complex partial) |
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Term
| diffuse brain involvement (both hemispheres). brief lapse of consciousness; pt usually unaware of attacks. brief staring episodes, eyelid twitching, NO post-ictal phase. may be clonic (jerking), tonic (stiffness) or atonic (loss of postural tone). MC in childhood ->usually ceases by 20y. EEG: bilateral symmetric 3Hz spike and wave action or may be normal |
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Definition
| absense (petit mal) nonconvulsive seizure |
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Term
tonic phase: loss of consciousness -> rigidity, sudden arrest of respiration (usually <60 sec) -> clonic phase. Clonic phase: repetitive, rhythmic jerking (lasts <2-3 minutes) -> postictal phase. postictal phase: flaccid coma/sleep: variable duration.
may be accompanied by incontinence, tongue biting or aspiration with postictal confusion. auras are prewarnings to seizures. EEG: generalize high-amplitude rapid spiking. may be normal in between seizures |
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Definition
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Term
| sudden, brief, sporadic involuntary twitching, No LOC. may be 1 muscle or groups of muscles |
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Definition
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Term
| "drop attacks"- sudden loss of postural tone |
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Definition
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Term
| repeated, generalized seizures w/o recovery >30 min |
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Definition
|
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Term
| paresthesias, numbness, pain, heat, cold, sensation of movement, olfactory, flashing lights (photopsia) |
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Definition
|
|
Term
| abdominal (nausea, vomiting, pain, hunger); cardiovascular (sinus tachycardia) |
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Definition
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|
Term
| treatment for absence (petit mal) seizures |
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Definition
| ethosuximids 1st line (only works for absence) valproic acid 2nd line (S/E hepatitis, pancreatitis), lamitrigine |
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Term
| treatment for grand mal seizures |
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Definition
| valproic acid, phenytoin, carbamazepine, lamotigine |
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Term
| treatment for status epilepticus |
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Definition
| lorazepam or diazepam -> phenytoin -> phenobarbital |
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Term
|
Definition
| valproic acid, clonazepam (febrile: phenobarbital) |
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Term
|
Definition
| lorazepam, diazepam, inc GABA |
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Term
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Definition
| blocks Na+ channels in the CNS (takes longer to work). S/E gingival hyperplasia, Steven Johnson Syndrome, hirsutism |
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Term
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Definition
| phenobarbital, binds to gaba receptors to inc BAGA-medicated CNS inhibition. prolactin levels are increased in seizures (helps to differentiate it from pseudoseizures). EEG help to establish the diagnosis and localize the lesions |
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Term
| most abundant excitatory neurotransmitter in CNS. released by upper motor neurons in the synapse to activate lower mostor neurons. also activates NMDA receptor. involved in normal brain function, memory, cognition and learning. inc in alzheimers, decreased in phenylketonuria |
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Definition
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Term
| most abundant inhibitory neurotransmitter in CNS. regulates muscle tone, protects against overexcitation (ex seizures). inc w ETPH, dec w upper motor neuron lesions, anxiety, huntington's disease |
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Definition
| GABA- gamma-aminobutyric acid |
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Term
| activates the muscle at the neuromuscular juntion (from the LMN to the effector cell (ex muscle) regulating movement. inc in parkinson disease, organophosphate poisoning- pesticides and sarin. decreased- alzheimer, huntington, major depression. botulism toxin (blocks acetylcholine release leading to paralysis) |
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Definition
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Term
| inhibitory CNS neurotransmitter, which allows for coordinated movement. smoothens movements. motivated behaviors (ex drug addiction), endocrine control, sexual behavior. inc in schizophrenia. dec in parkinson disease, depression, neuroleptic malignant syndrome, bromocriptine |
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Definition
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Term
| excitatory CNS neurotrasmitter. inc in anxiety, arousal, selective attention. dec in ADHD |
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Definition
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Term
| involved in regulation of mood, pain, higher cognition, emotion. inc in serotonin syndrome. dec in depression |
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Definition
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