uworld Neuro

Question 1

Elderly pt with impaired memory and executive disfunction

Answer 1

Late-life depression frequently presents with reversible cognitive impairment (pseudodementia)

Older adults with new-onset cognitive impairment should be assessed for depression.

Question 2

dementia vs psuedo dementia

Answer 2

clinical suspicion for depression, including his psychosocial situation, loss of interest and enjoyment, somatic symptoms, and anxious ruminations

Question 3

greatest risk of having late life depression

Answer 3

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

Question 4

head CT for head trauma

with or without contrast.

Answer 4

WITHOUT

contrast is most useful for identifying abscesses or intracranial masses, but contrast obscures acute bleeding

Question 5

Tuberous Sclerosis Complex

Answer 5

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.

Question 6

Clinical features of TSC (tuberous scleosis complex)

Answer 6

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

Question 7

Initial evaluation fo TSC

Answer 7

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

Question 8

leading cause of death in TSC

Answer 8

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.

Question 9

generalized convulsive status epilepticus

Answer 9

≥ 5 minutes of generalized convulsive seizure
OR
≥2 generalized convulsive seizures without interval recovery of consciousness

Question 10

TX GENERALIZED CONVULSIVE STATUS EPLIEPTICUS

Answer 10

1. Stabilize circulation, airway & breathing
2. Benzodiazepines (repeat administration until termination of seizure activity)
3. Begin antiepileptic drugs
4. EEG monitoring for refractory status epilepticus or failure to regain consiousness

Question 11

clinical presentation of cluster headaaches

Answer 11

-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

Question 12

tx cluster headache during an attack

Answer 12

first line abortive tx: 100% oxygen at 6-12 L/min for 15 min

-Sumatriptan (subcutaneous)
-Zolmitriptan nasal spray

Question 13

tx of cluster headache preventative

Answer 13

Verapamil
Lithium
Topiramate

Question 14

Triad:
1. Fever (~50%)
2. Focal/severe back pain
3. Neurologic findings (eg, motor/sensory change, bowel/bladder dysfunction, paralysis)

Answer 14

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

Question 15

neurologic progession in spinal epidural abscess

Answer 15

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

Question 16

Managment of spinal epidural abscess

Answer 16

confirm the diagnosis, suspected cases require urgent spinal MRI with contrast,

followed by antibiotics and surgical decompression to prevent neurologic sequelae and death.

Question 17

acute phenytoin toxicity

Answer 17

primarily affects cerebellum
(early): eye movement abnormalities (eg, nystagmus, blurry vision, diplopia)

(late): motor incoordination (eg, ataxia, dysarthria).

Question 18

window for fibrinolytic therapy in stroke

Answer 18

<4.5 hours from start of symptoms

Question 19

next step for stroke if not eligible for thrombolysis

Answer 19

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)

Question 20

cells for acustic neuroma

Answer 20

schwann cells (aka shwannomas)

Question 21

mechanism carotid artery dissection

Answer 21

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.

Question 22

sxs carotid artery dissection

Answer 22

1. Unilateral head & neck pain, transient vision loss
2. Ipsilateral partial Horner syndrome
   Ptosis & miosis without anhidrosis
3. Signs of cerebral ischemia (eg, focal weakness)

Question 23

management carotid artery dissection

Answer 23

1. Neurovascular imaging (eg, CT angiography)
2. Thrombolysis (if ≤4.5 hr after symptom onset) or Antiplatelet therapy (eg, aspirin) ± anticoagulation

Question 24

sxs of central pontine mylenosis

Answer 24

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

Question 25

mechanism of central pontine mylenosis

Answer 25

Overly rapid correction of hypotonic hyponatremia

Osmotic shock → oligodendrocyte death → demyelination

Highest risk: severe hyponatremia (≤120 mEq/L) of significant duration (>2days)

Question 26

delirum in the setting of dementia

Answer 26

fluctuations in consiousness

often only sign of acut ilness in dementia