-
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?
arteriography
-
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?
50-60 yo
-
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?
5-20 yo
-
What is the def of a generalized seizures vs partial seizure?
sudden loss of consciousness vs no loss of consciousness
-
jacksonian march
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
-
classic migraine
migraine with an aura
-
common migraine
migraine without aura
-
Migraine management
- 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)
-
selegiline
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
- pain
- autonomic dysfunction (tachycardia, cardiac irregularities, labile blood pressure, disturbed sweating, impaired plum function, spincter disturbances, or paralytic ileus)
-
Dx workup of guillan-barre syndrome
- EMG
- CSF (elevated protein, nl cell counts)
-
tx of guillan-barre syndrome
- hospitalized with close monitoring of respiratory status
- plasmapheresis
- IVIG
- PT/OT/ST
-
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
- EMG
- 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
-
Lambert-Eaton syndrome
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?
petechial rash
-
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)
-
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
gliomas
-
m/c spinal tumor
ependymoma
-
m/c sources of mets to the brain
lung, breast, kidney, and GI tract Ca
-
In what stage of sleep do nightmares occur?
REM
-
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?
clonazepam
-
How do you manage sleep terrors and sleep walking?
benzos
-
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
HSV
-
m/c childhood encephalitis
myxovirus (measles and mumps encephalitis)
-
Face feels stiff and pulled to one side with flattening of the nasolabial fold
Bell's palsy
-
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
- PT
- 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
corticosteroids
-
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?
corticosteroids
-
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
CVAs
|
|
