uworld Neuro Flashcards
Elderly pt with impaired memory and executive disfunction
Late-life depression frequently presents with reversible cognitive impairment (pseudodementia)
Older adults with new-onset cognitive impairment should be assessed for depression.
dementia vs psuedo dementia
clinical suspicion for depression, including his psychosocial situation, loss of interest and enjoyment, somatic symptoms, and anxious ruminations
greatest risk of having late life depression
Late-life depression (occurring age >65) has been found to be a significant risk factor for the development of major neurocognitive disorder (vascular or Alzheimer dementia) in the years that follow
head CT for head trauma
with or without contrast.
WITHOUT
contrast is most useful for identifying abscesses or intracranial masses, but contrast obscures acute bleeding
Tuberous Sclerosis Complex
Autosomal Dominant mutation in the hamartin (TSC1 gene) or tuberin (TSC2 gene) proteins that play a roll in cell division and differentiation.
Caauses benign tumors throughout the body, including the skin, CNS, heart and kidney.
Clinical features of TSC (tuberous scleosis complex)
Dermatologic:
Ash-leaf spots
Angiofibromas of the malar regionS
hagreen patches
Neurologic: CNS lesions (eg,subependymal tumors)
Epilepsy (eg,infantile spasms)
Intellectual disability
Autism & behavioral disorders (eg,hyperactivity)
Cardiovascular: rhabdomyomas
Renal: angiomyolipomas
Initial evaluation fo TSC
Thorough cutaneous examination, funduscopy, abdominal imaging and a brain MRI to evaluate for hamartomas. And baseline electroencephalogram.
if diagnosis is uncertain: genetatic testing for mutation in TSC1 or TSC2
leading cause of death in TSC
progressive, and neurologic impairment is the leading cause of death in patients with TSC.
Optimal seizure control is strongly associated with prolonged life span. For these reasons, a brain MRI and electroencephalogram should be obtained when TSC is initially diagnosed.
generalized convulsive status epilepticus
≥ 5 minutes of generalized convulsive seizure
OR
≥2 generalized convulsive seizures without interval recovery of consciousness
TX GENERALIZED CONVULSIVE STATUS EPLIEPTICUS
- Stabilize circulation, airway & breathing
- Benzodiazepines (repeat administration until termination of seizure activity)
- Begin antiepileptic drugs
- EEG monitoring for refractory status epilepticus or failure to regain consiousness
clinical presentation of cluster headaaches
-Short attacks (15-180 min) of severe unilateral orbital, supraorbital, or temporal pain
-Ipsilateral autonomic symptoms (eg, ptosis, miosis, lacrimation, conjunctival injection, rhinorrhea/nasal congestion)
-episodes are 6-12 weeks apart
tx cluster headache during an attack
first line abortive tx: 100% oxygen at 6-12 L/min for 15 min
-Sumatriptan (subcutaneous)
-Zolmitriptan nasal spray
tx of cluster headache preventative
Verapamil
Lithium
Topiramate
Triad:
1. Fever (~50%)
2. Focal/severe back pain
3. Neurologic findings (eg, motor/sensory change, bowel/bladder dysfunction, paralysis)
Spinal Epidural Abscess (a bacterial fluid collection in the epidural space)
SEA usually seen in bacteremia due to IV drug use or a distant infection (eg, endocarditis). ^ risk with immunocompromise
neurologic progession in spinal epidural abscess
Epidural space is a narrow so bacterial invasion tends to affect multiple adjacent spinal levels and to eventually compress the spinal cord.symmetric
progression:
1. Worsening focal back pain (eg, T10 spinal tenderness to palpation) →
2. Radicular nerve pain (eg, “shooting pains”) →
3. Sensory/motor/reflex deficits (eg, bilateral leg weakness, upgoing plantar reflexes) and bowel/bladder issues →
4. Paralysis
Managment of spinal epidural abscess
confirm the diagnosis, suspected cases require urgent spinal MRI with contrast,
followed by antibiotics and surgical decompression to prevent neurologic sequelae and death.
acute phenytoin toxicity
primarily affects cerebellum
(early): eye movement abnormalities (eg, nystagmus, blurry vision, diplopia)
(late): motor incoordination (eg, ataxia, dysarthria).
window for fibrinolytic therapy in stroke
<4.5 hours from start of symptoms
next step for stroke if not eligible for thrombolysis
CT angio head and neck looking for large vessel obstruction.
is no LVO or >24hrs then oral anti-platelet therapy. (eval for dysphagia if needed)
cells for acustic neuroma
schwann cells (aka shwannomas)
mechanism carotid artery dissection
intramural hematoma/thrombus in small caliber of the carotid artery result in luminal obstruction by the intramural blood collection.
Sympathetic nerves travel along the carotid artery, dissection may cause Horner syndrome (ie, ptosis, miosis, but anhidrosis usually missing) due to aneurysmal dilation and compression.
sxs carotid artery dissection
- Unilateral head & neck pain, transient vision loss
- Ipsilateral partial Horner syndrome
Ptosis & miosis without anhidrosis - Signs of cerebral ischemia (eg, focal weakness)
management carotid artery dissection
- Neurovascular imaging (eg, CT angiography)
- Thrombolysis (if ≤4.5 hr after symptom onset) or Antiplatelet therapy (eg, aspirin) ± anticoagulation
sxs of central pontine mylenosis
Locked-in syndrome*
1. Quadriplegia with intact consciousness
2. Upper CNs spared: intact vertical EOM, blinking & pupil reflexes
3. Lower CN paralyzed: loss of horizontal EOM & oral movements
mechanism of central pontine mylenosis
Overly rapid correction of hypotonic hyponatremia
Osmotic shock → oligodendrocyte death → demyelination
Highest risk: severe hyponatremia (≤120 mEq/L) of significant duration (>2days)
delirum in the setting of dementia
fluctuations in consiousness
often only sign of acut ilness in dementia
