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M/C type of stroke
ischemic stroke (80%)
What is the breakdown of the different types of ischemic stroke?
2/3 are thrombotic, 1/3 embolic
Where do emboli come from that cause strokes?
heart, aortic arch, or large cerebral arteries
What is the workup for a stroke?
CBC, ESR, platelet count, PT/PTT, cholesterol and lipids, and blood glucose level; CT scan; EKG
When can thrombolytics for strokes be given?
They are most effective within 3 hours, but can be attempted up to 12 hours
Contraindications to thrombolytics
- Suspicion of current bleed
- Recent intracranial surgery
- Serious head trauma or previous stroke
- Hx of heed bleed
- Bleeding problem
- Uncontrolled HTN (>185/110)
- Seizure at stroke onset
- internal bleeding
- brain tumor
- AVM or aneursym
- Heparin use within 48 hours
- Plt count <100,000
When do you initiate antiplt vs anticoagulant therapy?
Anti plt is for ischemic stroke and TIA, anti coag is for cardiac embolus
When are endarterectomies performed?
>70-90% stenosis of the common or internal carotid artery
How do you manage hemorrhagic stroke?
- conservative and supportive measures
- management of HTN and anti-edema therapy (mannitol and corticosteroids)
Pts with TIA related to carotids demostrate what type of sx?
contralateral hand-arm weakness with sensory loss, ipsilateral visual sx or aphasia, or amaurosis fugax
Those with vertebrovascular TIA experience what types of sx?
diplopia, ataxia, vertigo, dysarthria, CN palsies, lower extremity weakness, dimness or blurring of vision, perioral numbness, or drop attacks
What is the definitive study for TIA?
When do you initiate prophylactic antiplatelet therapy in a TIA? What type of meds are used?
When it is not cardiogenic; ASA, ticlopidine, clopidogrel, sulfinpyrazone, or dipyridamole
How do you tx a cardiogenic TIA?
anticoagulation, initially with IV heparin for those who are admitted to the hospital, and warfarin for long term therapy
What is the m/c nontraumatic cause of a subarachnoid hemorrhage?
ruptured berry aneurysm
What age range is m/c affected by subarachnoid hemorrhages?
When are AVMs m/c dx?
b/w 20-40 yo
S/sx of SAH
- "Worst HA of my life," N/V, AMS
- HA remains constant for days
- BP rises
- meningeal signs
What does CSF analysis show in SAH?
increased opening pressures and grossly bloody fluid
How do you tx SAH?
- provention of elevated arterial or ICP that might lead to rerupture of the vessel
- strict bed rest, mild sedation, or administration of stool softeners to prevent straining
At what ages do idiopathic seizures generally begin?
What is the def of a generalized seizures vs partial seizure?
sudden loss of consciousness vs no loss of consciousness
phenomenon with seizures whereisolated tonic activity of a limb speads to entire side of body
What is the difference between complex partial and simple partial seizures?
complex partial has an impairment of consciousness (ie, aura)
What do EEGs show in generalized absence seizures?
generalized spikes and associated slow waves
What does an EEG show in simple partial seizures?
focal rhythmic d/c at the onset of the seizure, but occsionally, no ictal activity will be seen
What does an EEG show in complex partial seizures?
interictal spikes or spikes associated with slow waves in the temporal or frontotemporal areas
How do you manage?
Correct any underly hypoglycemia, hyponatremia, or drug intoxication
What meds are used for generalized nonconvulsive seizures?
valproic acid or ethosuximide
Why is status epilepticus an emergency?
possibiliy of permanent brain damage secondary to hyperthermia, circulatory collapse, or excitotoxic neuronal damage
How do you manage status epilepticus?
Diazepam or lorazepam is administered IV until seizure stops, a loading dose of phenytoin or fosphenytoin is also given
What is the definition of MS?
inflammation associated with multiple foci of demyelination in the CNS white matter
What is the proposed cause of MS?
CNS IG production and alteration of T lymphocytes; a viral infection may act as a precipitant
What are sx of MS?
focal weakness, numbness or tingling, optic neuritis, diplopia, focal neuralgias, balance problems, or urinary sx
what does CSF show in MS?
sterile inflammation with mild lymphocytosis or slight protein elevation, elevated IG index, oligoclonal bands, and increased myelin basic protein
How do you manage MS?
- High dose steroids
- Interferon B to decrease frequency of relapse
- daily sub-q injections of glatiramer acetate to decrease frequency of relapses
- Amantadine and pemoline for fatigue
- Baclofen and diazepam for spasticity
Pathology of alzheimers
intracellular neurofibrillary tangles and extracellular neuritic plaques
What are the four ACH inhibitors?
tacrine, donezepil, galantamine, or rivastigmine
Sx of vascular dementia
- forgetfulness in the absence of depression and inattentiveness
- sx occur in STEPWISE fashion
- Social graces may be well maintained
- Progression leads to loss of computational ability, problems with word finding and concentration, difficulty with routine daily activities, and complete disorientation and social withdrawal
What is the pathophys of tension HA?
abnl neuronal sensitivity, muscle contraction, stress or minor trauma to head and neck
How do you manage tension HA?
ASA, APAP, or NSAIDs; local heat and relaxants
Sx of migraine HA
U/L pain with throbbing or pulsing discomfort
Pathophys of migraines
intracranial vasopasm followed by extracranial vasodilation; dysfunction of the trigeminovascular system, resulting in the perivascular release of substance P
migraine with an aura
migraine without aura
- ASA, APAP, NSAIDs, or isometheptene
- Triptans or ergotamines
- Prophylaxis: Beta blockers, TCAs, CCBs, NSAIDs, valproic acid, or topiramate
- botox in pts with severe, intractable, migraines
Pathophys of benign essential tremor
idiopathic, inherited in autosomal dominant manner
Management of essential tremor
propanolol at low doses; may try primidone if propanolol fails
pathophys of Parkinson's disease
degeneration of cells in the substantia nigra, causing a deficiency of the neurotransmitter dopamine, and an imbalance of dopamine and acetylcholine
Why is levodopa used in parkinsons?
It is the precursor to dopamine
What is the main direction of parkinson's tx?
to restor balance between dopamine and acetylcholine by blocking the effect of acetylcholine with anticholinergic drugs, adminstering levodopa (precursor of dopamine) or a combo of both
What is amantadine?
an anticholinergic, good for parkinson's sx, specifically tremor, but not rigidity
What is carbidopa?
A drug used in Parkinson's that lowers doses of carbidopa and reduces side effects
How do you tx parkinson's pts when they become refractory to levodopa therapy?
dopamine agonists (like bromocriptine)
MAO-B inhibitor, inhibits breakdown of dopamine, may arrest progression of the disease
genetics of huntington's disease
autosomal dominant disorder
gene resposible for huntington's disease
short arm of chromosome 4
earliest signs of huntington's
mere restlessness or fidgetiness
What can RLS be secondary to?
peripheral neuropathy, uremia, pregnancy, IDA
When do sx of RLS occur?
during periods of prolonged inactivity
drug sof choice for RLS
dopamine agonists or ropinirole
epidemiology of Bell's palsy
pregnant women and people with diabetes
How do you manage Bell's Palsy?
PO course of prednisone with or without acyclovir
M/c type of diabetic peripheral neuropathy
mixed (motor, sensory, and autonomic)
what is guillan-barre syndrome?
an idiopathic polyneuropathy often following minor infections, immunizations, or surgical procedures, but in many cases, no cause is identified
pathogen associated with guillan-barre syndrome
campylobacter jejuni, usually with infection of lungs or GI tract
Clinical features of guillan-barre syndrome
- symmetrical extremity weakness that begins distally and ascends; promximal muscles affected more than distal muscles; decreased or absent DTRs
- autonomic dysfunction (tachycardia, cardiac irregularities, labile blood pressure, disturbed sweating, impaired plum function, spincter disturbances, or paralytic ileus)
Dx workup of guillan-barre syndrome
- CSF (elevated protein, nl cell counts)
tx of guillan-barre syndrome
- hospitalized with close monitoring of respiratory status
Epidemiology of myasthenia gravis
m/c in young women and older men
pathophys of myasthenia gravis
Abs directed against the ACH receptor on the muscle surface cause an increased rate of receptor destruction, leading to weakness
Clinical features of myaesthenia gravis
- muslce weakness and fatiguability which improve with rest
- Ptosis, diplopia, difficulty in chewing or swallowing, respiratory difficulties, limb weakness
- sx fluctuate in intensity throughout the day, and there is a tendency to have longer-term spontaneous relapses and remissions that may last for weeks
How do you dx myasthenia gravis?
clinical improvement is seen after adminstering anticholinesterase (edrophonium)
Workup of myasthenia gravis
- CXR to r/o coexisting thymoma
- Serum assay for elevated levels of Abs (positive in 80-90% of pts)
Tx of myasthenia gravis
- give cholinesterase inhibitor such as pyridostigmine
- thymectomy leads to improvement of sx
- corticosteroids, immunosuppressive agents, IVIG, and plasmapheresis in pts with refractory dz
defective relase of ACH in response to nerve impulse, associated with small cell carcinoma, may surface prior to tumor being dx
How does Lambert-Eaton syndrome differ from myasthenia gravis?
power increases with sustained contraction
How do you dx Lambert-Eaton syndrome?
EMG, as muscle response to repeated stimulation is increased significantly
How do you tx Lambert-Eaton syndrome?
- plasmapheresis and immunosuppressive therapy
- specific therapy on the tumor
M/C cause of meningitis in infants
Group B strep
typical s/sx of meningitis
Fever, HA, vomiting, and a stiff neck are the typical signs and sx
What rash is characteristic of Neisseria meningitidis?
Workup of meningitis
- CT performed BEFORE LP to r/o mass
- Gram stain and culture of CSF
Management of neonatal meningitis
ampcillin and cefotaxime
Management of infantile meningitis
Ampicilllin + cefotaxime OR rocephin
Management of meningits b/w 3 mo and 55 years
Cefotaxime or ceftriaxone plus vanco
Management of meningitis in adults >55 or immunocompromised
amp plus vanco plus cefotaxime or ceftriaxone
What should be seen with effective management of meningitis?
- Repeat LP and CSF analysis; CSF sould be sterile after 24 hours
- Decrease in pleocytosis and proportion of neutrophils should be seen within three days
M/C cause of viral meningitis
enteroviruses (coxsackievirus A or B, echoviruses), HSV2, and arthropod-borne viruses
Difference in s/sx b/w viral and bacterial meningitis
- bacterial is more acute; viral persists for days
- lots of systemic manifestations (rash, pharyngitis, adenopathy, pleuritis, carditis, jaundice, organomegaly, diarrhea)
difference in CSF b/w bacterial and viral meningitis
- CSF opening pressure nl in viral, increased in bacterial
- nl or high nl WBCs in viral
- protein, glucose, and serum blood counts are nl
Management of viral meningitis
- None needed, if HSV, give acyclovir
- tx mild HA with APAP
Tx of increased ICP
hyperventilation, IV mannitol infusion, and iv furosemide
sx of total cord transection
- immediate, flaccid paralysis and loss of sensation below the level of the lesion
- reflex activity is lost for a variable time, urinary and fecal retention
- with slow return of reflex function, spatic paraplegia or quadriplegia develops, with hyperreflexia and extensor plantar responses
Sx of partial cord injury
- mild limb weakness or distal sensory disturbance
- sphincter function impairment may lead to incontinence and urgency
Sx of U/L cord lesion
ipsilateral motor disturbance with accompanying impairment of propioception and C/L loss of pain and temp below the lesion (aka Brown-Sequard syndrome)
ipsilateral motor disturbance with accompanying impairment of propioception and C/L loss of pain and temp below the lesion
sx of central cord lesions
LMN deficit and loss of pain and temp, with a sparing of posterior column functions
sx of radicular deficit
occurs at level of injury
managment of cord injuries
- immobilization, decompressive laminectomy and fusion if there is cord compression
- high dose corticosteroids within 8 hours of injury will help with recovery
m/c type of brain tumor
m/c spinal tumor
m/c sources of mets to the brain
lung, breast, kidney, and GI tract Ca
In what stage of sleep do nightmares occur?
In what stage of sleep do sleep terrors occur?
Stage 3 and 4 delta sleep
In what stage of sleep do sleep walking occur?
stage 3 or 4 sleep in the first third of the night and with REM sleep later on in the night
In what stage of sleep does nocturnal enuresis occur?
within 3-4 hours of falling asleep, not associated with any particular changes
How do you manage narcolepsy?
administration of stiulants including dextroamphetamine and modafinil
How do you manage nocturnal myoclonus?
How do you manage sleep terrors and sleep walking?
What parts of the brain are affected by Alzheimers?
hippocampus, neocortex, and nucleus basalis
m/c initial sx of alzheimers
memory impairment for newly acquired information with memory for remote events unimpaired
What is tabes dorsalis?
late complication of tertiary syphilis, characterized by spirochete invasion of the posterior columns of the spinal cord
Argyll - Robertson pupils
pupils react poorly to light but well to accomodation
Management of neurosyphilis
IV aqueous PCN G at 18-24 U/day x10-14d
m/c cause of viral encephalitis
m/c childhood encephalitis
myxovirus (measles and mumps encephalitis)
Face feels stiff and pulled to one side with flattening of the nasolabial fold
Age of onset of Duchenne's MD
infancy of early childhood, death usually during adolescence
Age of onset of Becker's MD
Childhood, adolescence, or early adult; death usually occurs in 5th decade, but some have nl lifespan
Age of onset of Myotonic MD
early adult onset, slow progression, most pts are confined to a wheelchair or bed within 15-20 years
Pattern of muscular specific features of duchenne's MD
pelvic-femoral, later on pectoral girdle
Pattern of muscular specific features of Becker's MD
pelvic-femoral; later on pectoral girdle
Pattern of muscular specific features of myotonic MD
ocular, facial; sternomastoid; forearm peroneal; cardiac involvement common
Sx of Duchenne's MD
pseudohypertrophy, respiratory and cardiac involvement; mental retardation
Sx of becker's MD
Slight cardiac involvement, nl mentation
Sx of Myotonic MD
Cataracts; testicular atrophy, alopecia
Pathology of MD
- necrosis of muscle fibers and gradual replacement of fibers with CT and fat; loss of muscle fibers, residual fibers of larger and smaller size than nl in hapzard arrangement;
- Genetic abnormality (x chromosome) causing dystrophin, a muscle protein, to be absent in Duchenne's dystrophy....results in loss of membrane proteins and initiation of the degeneration of muscle fibers
clinical features of MD
symmetrical muscle weakness atrophy, contractures, ptosis, dysphagia, mental retardation, myotonia, cataracts, testicular atrophy, alopecia, and cardiac involvement
Workup of MD
EMG, serum CK (highest in duchenne's), muscle bx, dystrophin analysis, genetic analysis
Management of MD
- No specific tx
- Steroids and quinine (for myotonia)
- Pneumococcoal vaccine and annual influenzae vaccine
- ACE Is, BBs, and annual echo
- corticosteroids are mainstay > 5 yo
asterixis, and how to do tx
- flapping of outstretched hands d/t increased ammonia levels
- tx with lactulose
Which of medication is an acceptable first-line agent to reduce the frequency and severity of recurrent exacerbations and disease progression in a patient with newly diagnosed multiple sclerosis?
Interferon B (corticosteroids are used for acute attacks, but do not alter course of disease)
preventative medications for cluster HA
Which medication, if started within five days of symptoms, has been shown to increase the rate of full recovery in an acute Bell's palsy patient?
Tramadol should be avoided in seizure disorder because
it lowers the seizure threshold
central cord syndrome
- loss of motor function that is more severe in the upper extremities than in the lower extremities, and is more severe in
- the hands.
- There is typically hyperesthesia over the shoulders and arms.
Women who suffer from migraine with aura are at increased risk for
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