Neurology

Question 1

Migraine abortive therapy

Answer 1

• Simple analgesics (eg, NSAIDs, acetaminophen)
• Antiemetics (eg, metoclopramide, prochlorperazine)
• Triptans (eg, sumatriptan)
• Ergotamine, dihydroergotamine
• CGRP receptor antagonists (eg, rimegepant)

Question 2

Migraine preventive therapy

Answer 2

• Antiepileptics (eg, topiramate, divalproex sodium)
• Tricyclic antidepressants (eg, amitriptyline)
• Beta blockers (eg, propranolol)
• CGRP monoclonal antibodies (eg, erenumab)

Question 3

Chronic inflammatory demyelinating polyradiculoneuropathy

Answer 3

presents with progressive muscle weakness, distal sensory loss, and diminished or absent reflexes developing over >8 weeks.

Diagnosis is confirmed with electrodiagnostic studies demonstrating peripheral nerve demyelination.
Cerebrospinal fluid analysis will show albuminocytologic dissociation in the vast majority of cases.

Question 4

Idiopathic intracranial hypertension (IIH) (ie, pseudotumor cerebri).

Presentation

Answer 4

Symptoms of IIH include headaches, visual symptoms, tinnitus, and diplopia.

Headaches are chronic, holo-cranial, and pulsatile in nature; they are exacerbated by lying flat and improved by sitting up.

The most important sign of IIH is papilledema, which is frequently bilateral and can lead rapidly to vision loss.

Question 5

Idiopathic intracranial hypertension (IIH) (ie, pseudotumor cerebri).

Risk factors

Answer 5

frequently seen in young obese women, it has also been associated with certain medications (eg, isotretinoin, tetracyclines, growth hormone, and vitamin A).

Question 6

Idiopathic intracranial hypertension (IIH) (ie, pseudotumor cerebri).

Diagnosis

Answer 6

Diagnosis of IIH includes
-complete ocular examination

-neuroimaging to exclude secondary causes of intracranial hypertension (eg, mass, hemorrhage, cerebral vein thrombosis).

*Empty sella is present in about 70% of patients with IIH but is not diagnostic.

Lumbar puncture is performed with the patient in the lateral decubitus position. An opening pressure of > 250 mm H₂O is considered abnormal.
CSF studies are normal in IIH patients.

Question 7

Idiopathic intracranial hypertension (IIH) (ie, pseudotumor cerebri).

Treatment

Answer 7

• weight loss
• headache prophylaxis with topiramate
• acetazolamide (+/- furosemide).

Short-term treatment may involve corticosteroids and serial lumbar punctures for patients awaiting surgery for progressive visual loss.

Surgical choices include optic nerve sheath fenestration and/or CSF shunting procedures

Question 8

3rd Cranial nerve palsy, Non pupil sparing

Answer 8

Non-pupil-sparing third nerve palsies are frequently caused by mass effect (eg, intracranial aneurysm, tumor). Aneurysms arise from vessels that have a close anatomic relationship with the third nerve (eg, posterior cerebral artery, superior cerebellar artery, posterior communicating artery). A non-pupil-sparing third nerve palsy (as seen in this patient) should be considered due to an aneurysm until proved otherwise; patients should undergo immediate MR or CT angiography for evaluation.

Question 9

3rd Cranial nerve palsy, Pupil sparing

Answer 9

Pupil-sparing third nerve palsies are typically caused by microvascular ischemia;

they are associated with diabetes, hypertension, hyperlipidemia, and advanced age.

Observation and supportive care may be appropriate in patients with vasculopathic risk factors (eg, diabetes, hypertension),
although some physicians advocate for imaging to exclude mass effect with all third nerve palsies

Question 10

Meralgia paresthetica

Answer 10

is due to lateral femoral cutaneous nerve (LFCN) compression

presents with pure sensory symptoms (e.g., numbness, paresthesias, and dysesthesias) in the anterolateral thigh.
Risk factors include wearing tight pants or belts, pregnancy, obesity, and diabetes.
The diagnosis is made clinically.
Patients should be reassured that this is not a serious condition, and they usually respond to conservative treatment

Question 11

Thrombotic vs Embolic stroke in clinical presentation

Answer 11

Ischemic strokes may be caused by embolism or thrombosis.
Embolic strokes usually have an abrupt onset of focal neurologic findings with maximal symptoms at onset.
Thrombotic strokes usually present as fluctuating symptoms with periodic improvement and a stuttering progression

Question 12

Brain lesions and prophylactic anti-convulsant

Answer 12

Current studies show prophylactic anticonvulsant medications are mainly beneficial in:
⏩⏩patients with newly diagnosed brain tumors who present with a seizure.
⏩⏩Prophylactic anticonvulsants (for 1 week with taper afterwards) are also indicated in patients who have had a craniotomy for brain tumor resection, brain MRI showing acute hemorrhage within the tumor, or significant mass effect/edema in the vicinity of the cortex.

Question 13

Brain lesions management

Answer 13

Patients presenting with new-onset headache with focal neurologic deficits in the setting of cerebral metastatic disease should be started on intravenous steroids (e.g., methylprednisolone or dexamethasone) to reduce vasogenic edema and mass effect.

Question 14

Restless leg syndrome
Manafistation

Answer 14

Uncomfortable urge to move legs with:
• Unpleasant sensations in the legs
• Onset with inactivity or at night
• Relief with movement (eg, walking, stretching)

Question 15

Restless leg syndrome
Risk factors & associated conditions

Answer 15

• Iron deficiency
• Uremia
• Pregnancy
• Diabetes mellitus (especially with neuropathy)
• Multiple sclerosis, Parkinson disease
• Drugs: antidepressants, antipsychotics, antiemetics

Question 16

Restless leg syndrome
Management

Answer 16

Non-pharmacologic Limit caffeine & alcohol Regular, moderate exercise. Warm &/or cold soaks or compresses

Pharmacologic
-Supplemental iron (if serum ferritin <75 ng/mL)

• Mild intermittent symptoms: carbidopa-levodopa as needed
  • Frequent/daily symptoms: a28 calcium channel ligand (eg, gabapentin, pregabalin)
  • Dopamine agonists (eg, pramipexole, ropinirole) not preferred

Question 17

TIA disposition

Answer 17

Patients with recent (within 24-48 hours) transient ischemic attack (TIA) and risk factors:
-multiple recurrent TIAs,
-atrial fibrillation,
-symptom duration > 1 hour,
-symptomatic internal carotid artery stenosis > 50%,
-hypercoagulable disorders, or
-high ABCD² score

have higher risk of stroke within the next 48 hours. They should be hospitalized for further investigation and prevention.

Question 18

Upper motor neurons signs

Answer 18

• Spastic paralysis
• Clasp-knife rigidity
• Hyperreflexia
• Babinski sign

Question 19

Lower motor neurons signs

Answer 19

• Flaccid paralysis
• Hypotonia
• Hyporeflexia
• Muscle atrophy & fasciculations

Question 20

Parkinson disease pharmacologic therapy

Answer 20

Levodopa/carbidopa: Most effective, preferred in severe disease & patients age >65 due to motor fluctuations in younger patients

Dopamine agonists: (Pramipexole) Preferred in patients age <65 & with mild to moderate disease

Anticholinergics (Trihexyphenidyl): Can be used in patients age <70 with tremor & no significant akinesia or gait disturbance

Question 21

Brain death testing

Answer 21

When clinical criteria suggest brain death, the best next step is apnea testing. Patients must be hemodynamically stable with a body temperature > 36 C (97 F), normal pH, and normal PaCO2/PaO, levels. Apnea testing objectively confirms brainstem failure if

the patient cannot generate spontaneous breaths or trigger the ventilator in response to elevated PaCO, levels > 10 minutes after disabling control mode

Question 22

Dementia with lewy bodies management

Answer 22

Pharmacotherapy for DLB includes cholinesterase inhibitors for cognitive impairment, melatonin for RBD, and carbidopa-levodopa for parkinsonism. Patients with DLB are extremely sensitive to antipsychotics; as a result, low-potency, second-generation antipsychotics (eg, quetiapine) should be used only for functionally impairing hallucinations or delusions.

Question 23

Valproate toxicity

Answer 23

Valproic acid can lead to elevated serum ammonia levels resulting in encephalopathy. Patients presenting with encephalopathy on valproic acid should have their serum ammonia and valproate levels checked. Treatment includes discontinuing the drug and starting lactulose. L-carnitine can also be considered.

Question 24

Single unprovoked seizure

Answer 24

single unprovoked seizure requires investigation with laboratory studies, MRI of the brain, and EEG to rule out underlying organic disease and estimate future seizure risk. Abnormal studies indicate a high risk of recurrence and usually require antiepileptics.

Question 25

Para neoplastic cerebellar degeneration

Answer 25

A) PCD is most commonly associated with lung, gynecologic, and breast cancer.
B)Patients classically present with the acute onset of dizziness with nausea/vomiting, followed by cerebellar signs, dysarthria, and diplopia several days later.
C)Symptoms may progress over weeks to months and often precede a cancer diagnosis by years,
D) MRI may initially be normal but can demonstrate cerebellar atrophy with prominent cerebellar folia several months after symptom onset.
E)Cerebrospinal fluid analysis may show mild pleocytosis and elevated protein. Paraneoplastic antibodies (eg, anti-Yo, anti-Hu, anti-Ri) are helpful in confirming PCD, but negative results do not exclude the diagnosis.
F)Patients without a diagnosis of cancer should undergo workup for occult malignancy.

Question 26

Medications overuse headache

Answer 26

Medication-overuse headache (MOH) can present in the setting of a primary chronic headache disorder. It needs to be addressed separately from the chronic headache disorder by the discontinuation of the offending analgesic agent and the introduction of a short oral steroid taper.

Question 27

REM sleep behavior treatment

Answer 27

sleep environment to minimize injury (eg, removing sharp and breakable objects, placing a cushion next to the bed) .

Melatonin is preferred as first-line treatment due to its favorable side-effect profile.

Low-dose clonazepam is an effective augmentation or alternative therapy for refractory cases.

Question 28

Atrial fibrillation anticoagulation in patients with high risk of bleeding

Answer 28

In patients with atrial fibrillation who are at high risk of stroke and cannot tolerate oral anticoagulation therapy, left atrial appendage occlusion is effective for stroke prevention.

Occlusion can be achieved percutaneously with a self-expanding device that is implanted in the left atrial appendage or with surgical closure.

It is important to note that oral anticoagulation is recommended for the first 45 days after device occlusion of the left atrial appendage

Question 29

Transverse myelitis
Presentation

Answer 29

Rare inflammatory disorder causing segmental spinal cord injury. Most cases of TM are idiopathic, likely due to an autoimmune process following a viral infection (50% of cases).

Patients present initially with spinal shock - lower-extremity weakness, flaccidity, areflexia, and absent Babinski sign. There will be a sensory level to all primary sensory modalities. Bowel and bladder dysfunction are present. Some patients also complain of a “band-like” squeezing pain. After 1 week, patients usually develop spasticity, hyperreflexia, Babinski sign, and clonus.

Question 30

Transverse myelitis
Diagnosis and treatment

Answer 30

Diagnosis is suggested by magnetic resonance imaging with contrast, which shows enhancing cord segments with surrounding edema. Cerebrospinal fluid analysis usually shows elevated protein, moderate lymphocytosis, normal glucose, and no oligoclonal bands. Treatment is typically supportive (physical therapy). Intravenous corticosteroids can sometimes help patients with an autoimmune component of the disease.
Recovery usually occurs within 3 months, with up to 40% of patients experiencing some residual disability.

Question 31

Intracranial radiation complications

Answer 31

Patients who received intracranial irradiation (e.g., childhood ALL) are at an increased risk of developing brain tumors (primarily meningiomas) after a prolonged latency period.

Question 32

Peripheral neuropathy workup approach

Answer 32

Diagnostic evaluation of peripheral neuropathy should be considered in patients when the etiology of neuropathy is unclear or in the setting of severe or rapidly developing symptoms. The initial workup may include laboratory studies such as blood glucose, vitamin B12, TSH, antinuclear antibody, rapid plasma reagin, hemoglobin A1c, erythrocyte sedimentation rate, complete blood count, and serum protein electrophoresis.

Question 33

Foot drop deferential

Answer 33

A) Common peroneal nerve compression: Weakness of foot dorsiflexion, eversion, and toe extension. Pain is uncommon.

B) L5 radiculopathy: More extensive weakness involving foot dorsiflexion, eversion, and inversion; toe extension; and possible weakness of leg abduction. Back pain radiating down the leg is common.

Sensation may be decreased along the lateral leg and dorsum of the foot in both disorders, and reflexes are typically normal.

Question 34

Acute dystonia

Answer 34

Acute dystonic reactions can be caused by antidopaminergic agents (eg, metoclopramide). Treatment involves discontinuation of the drug and administration of anticholinergic agents (eg, benztropine, trihexyphenidyl) or agents with both anticholinergic and antihistamine effects (eg, diphenhydramine).

Question 35

Cerebral amyloid angiopathy

Answer 35

CAA is the second most common cause of ICH and is due to infiltration of cerebral blood vessels with an abnormal beta-pleated sheet protein (amyloid), which causes the blood vessels to lose their natural elasticity and become more fragile and bleed easily.
Most patients are asymptomatic but may present with transient neurologic symptoms (eg, weakness, paresthesias) or, more commonly, symptoms of spontaneous lobar ICH (eg, headache, focal deficits or hemiparesis, seizures, altered mental status).

CAA is probable in patients age >75 with multiple lobar (ie, cortical and subcortical white matter) hemorrhages on brain imaging.

Hemorrhage usually spares the ventricles and deep brain structures (eg, putamen, thalamus, pons).

Question 36

CVT and IBD (UC)

Answer 36

Ulcerative colitis, particularly, is associated with an increased risk of cerebral venous sinus thrombosis, which may be related to a systemic inflammatory state or other factors.
The diagnosis of cerebral venous sinus thrombosis should be considered in patients with ulcerative colitis with unexplained headache.

Question 37

Peripheral Neuropathy associated Acromegaly

Answer 37

Pts with acromegaly are at risk for multiple neurologic & neuromuscular effects, including median and ulnar neuropathies.
At present, the pathophysiology of these syndromes is felt to be peripheral nerve edema; this is important because the nerve edema and associated compressive neuropathy symptoms tend to improve with correction of growth hormone excess.

Question 38

Wernicke encephalopathy (thiamine deficiency) “CANO”

Answer 38

Cognitive changes, Ataxia, Nystagmus & Ocular movements disturbances

To avoid Wernicke encephalopathy in pts who might be at risk for the condition, thiamine should be administered before IV fluids with glucose

Question 39

Atypical parkinsonism Clues

Answer 39

A)Progressive supranuclear palsy:
Abnormal eye movements with prominent vertical gaze palsy

B)Lewy body dementia
Early progressive dementia with visual hallucinations

C)Corticobasal degeneration
Apraxia

D)Multiple system atrophy
Early prominent dyskinesia + Autonomic dysfunction (Orthostatic Hypotension)

E)Normal pressure hydrocephalus
Triad: Gait dysfunction, Dementia, and Urinary incontinences

F)Vascular parkinsonism
LL parkinsonism > UL, with Risk factors for Vascular insults

Question 40

Pharmacotherapy for Essential Tremor

Answer 40

First Line:
#Propranolol (both short- and long-acting formulations)
#Primidone (with or without propranolol)

Second Line:
#Other β-blockers (e.g., metoprolol, atenolol)
#Anticonvulsants (e.g., gabapentin, topiramate)
#Benzodiazepines (e.g., alprazolam, clonazepam, lorazepam)

Question 41

Trigeminal Neuralgia pearls

Answer 41

Neurovascular compression is the cause of most cases of TN > 50 years.

Most often a vascular loop is indenting the trigeminal nerve root and causes the classic unilateral neuralgic pain of TN.

Multiple sclerosis is the most common cause of TN < 40 years.

Multiple sclerosis patients are at a 20 times higher risk of TN compared to the general population.

Question 42

treatment for out-of-hospital repetitive seizures or status epilepticus

Answer 42

Intranasal or buccal midazolam is regarded as the first-choice treatment for out-of-hospital repetitive seizures or status epilepticus.

Question 43

Antibiotics to avoid in Myasthenia patients

Answer 43

Fluoroquinolones & aminoglycosides are common offenders, the former carries a US FDA boxed warning for use in pts with MG.

Question 44

Miller-Fisher syndrome (MFS)

Answer 44

Observed in about 5% of all cases of GBS.

#Classically presents as a triad of:
1) Ataxia, 2) Areflexia, and 3) Ophthalmoplegia.
#Acute onset of external ophthalmoplegia is a cardinal feature.
#Ataxia out of proportion to the degree of sensory loss.
#+ve GQ1b ganglioside.

Question 45

When to intubate MG or GBS patients presenting with respiratory distress

Answer 45

Vital Capacity(VC) < 20ml\kg (<~1L)
or
Max inspiratory pressure(MIP) > -30mmHg
or
Max expiratory pressure(MEP) <40mmHg

Question 46

Lambert-Eaton Myasthenic Syndrome triad

Answer 46

1)Proximal muscle weakness
2)Hyporeflexia\ Areflexia
3)Autonomic dysfunction

Question 47

Toxin (i.e. Drug) induced myopathy

Answer 47

Associated with Normal CK level, Normal EMG, biopsy show Type 2 Fibers atrophy.

In Contrast, HCQ, Statins, alcohol, and Colchicine are associated with elevated CK levels.

HCQ and colchicine biopsy will show vacuoles

Question 48

Alemtuzumab and Herpes prophylaxis (Acyclovir)

Answer 48

Alemtuzumab binds CD52 and depletes B cells, T cells, natural killer cells, and monocytes.
Prophylaxis with acyclovir reduces the incidence of herpesvirus reactivation but does not fully prevent this; several patients still develop herpes simplex virus and varicella-zoster virus infections

Question 49

Neuromyelitis Optica Spectrum Disorders
Definition

Answer 49

inflammatory disorders (has a relapsing course in 90 % of cases) of the CNS characterized by severe, immune-mediated demyelination and axonal damage predominantly targeting:
A)Optic nerves
B)Spinal cord
C)Brainstem > brain

NMO and NMOSD are distinguished from MS & other CNS inflammatory disorders by the presence of the disease-specific AQP4 Abs

Question 50

Neuromyelitis Optica Spectrum Disorders
Treatment

Answer 50

1)Acute plan: high-dose IV methylprednisolone (1g/d x 5) or PLEX

2)Intermediate plan: oral steroid (0.75 – 1mg/Kg)

3)Long term plan: Immunosuppression for relapse prevention with Azathioprine, Mycophenolate mofetil, Rituximab, Methotrexate

Question 51

Herpes Zoster complication

Answer 51

Varicella-zoster virus vasculopathy of one or more of the large intracerebral arteries is a recognized complication of herpes zoster ophthalmicus.

Cranial neuropathy, such as facial palsy, is a recognized complication of zoster oticus, in which the geniculate ganglion is the site of virus reactivation.

Question 52

Signs of Vitamin E deficiency

Answer 52

Ophthalmoplegia, retinopathy, spinocerebellar syndrome with peripheral neuropathy (with signs of cerebellar ataxia)

Question 53

Carcinomatous meningitis

Answer 53

Carcinomatous meningitis involves widespread malignant seeding of the leptomeninges, and evidence of leptomeningeal enhancement may be present on brain MRI.

CSF findings may include:
-Elevated opening pressure
-Increased leukocyte count
-Increased protein
-Decreased glucose

Question 55

Ideopathic intracranial hypertension pearls

Answer 55

• Increased intracranial pressure in the absence of any vascular or space-occupying lesion is the hallmark of idiopathic intracranial hypertension.

• Idiopathic intracranial hypertension is associated with use of tetracyclines, retinoic acid, and progesterone or estrogen supplements; discontinuation of any potential offending agent is the first step in management

Question 56

Tension type headache prevention

Answer 56

• Nonpharmacologic treatment strategies, such as relaxation training and cognitive behavioral therapy, should be considered for all patients with tension-type headache.

• Amitriptyline is the only agent that has been shown to be effective in the prevention of tension-type headache in controlled clinical trials.

Question 57

Creutzfeldt Jakob disease

Answer 57

• Creutzfeldt-Jakob disease is a prion-related disorder that often presents with rapidly progressive dementia.

• The real-time quaking-induced conversion assay is the most sensitive and specific test for prion proteins in the cerebrospinal fluid.

Question 58

Medications overuse headache

Answer 58

• Medication overuse headache can result from the use of triptans, ergot alkaloids, opioids, or combination analgesics for 10 or more days per month or simple analgesics for 15 or more days per month.

• Treatment of medication overuse headache is to wean overused acute medications, initiate migraine preventive medication, and provide new acute medications limited in use to 10 or fewer days per month.

Question 59

Orthostatic hypotension in Parkinson patients

Answer 59

🔴Orthostatic hypotension in Parkinson disease can be due to disease related autonomic dysfunction, comorbidities (such as diabetic autonomic neuropathy), or a peripheral effect of levodopa.
🔴Symptom onset after initiation of levodopa therapy should alert clinicians to this potential drug-related adverse effect.
🔴Carbidopa blocks the adverse effects of levodopa outside the brain and is always administered in combination with levodopa. However, in patients with severe peripheral side effects of levodopa, such as orthostatic hypotension, higher carbidopa doses can alleviate these symptoms.

🔴Droxidopa and fludrocortisone can be used for symptomatic management of neuro genic orthostatic hypotension and would be the appropriate next options if additional carbidopa is ineffective.
However, unlike carbidopa, these medications are associated with risk for supine hypertension; therefore, a carbidopa trial should be prioritized.

Question 60

Intracranial aneurysms

Answer 60

• Risk for rupture at 5 years is low for unruptured intracranial arterial aneurysms less than 7 mm in the posterior circulation and less than 12 mm in the anterior circulation.

• Annual noninvasive imaging is recommended in patients with an unruptured aneurysm.

Factors associated with increased risk for rupture include rapid growth detected over serial imaging, active tobacco use, previous aneurysm rupture and uncontrolled hypertension

Question 61

Elevated ICP management

Answer 61

Emergent treatment includes elevation of the head of the bed to 30 degrees, hyperventilation (usually with mechanical ventilation) to an arterial Pco, of 20 to 25 mm Hg (2.7-3.3 kPa), infusion of either hypertonic saline or mannitol , and administration of dexamethasone (for patients with peritumoral edema).
These treatments can be life-saving and often are used as a bridge to emergent surgery

Question 62

Anti-convulsant with skin rash

Answer 62

In addition to lamotrigine, phenobarbital, phenytoin, and carbamazepine (Options A, C, and D) are all known to cause rash. The rash may be severe and life-threatening and occur at an incidence high enough that these drugs should be avoided, especially in patients with prior drug rash (owing to cross-reactivity), unless no other good medication options are available
Gabapentin is a first-line medication for treating epilepsy in older adults; it has a low incidence of rash and other allergic reactions and good evidence of efficacy

Question 63

When to proceed to surgery in spinal cord compression

Answer 63

• In patients with metastatic spinal compression, surgical decompression should be reserved for patients younger than 65 years with a single area of compression, paraplegia for less than 48 hours, and a predicted survival of longer than 6 months.

Question 64

Migraine and ocps

Answer 64

In the absence of aura, there is no indication to discontinue estrogen-containing oral contraceptives in patients with migraine headaches.

Question 65

Treatment of fronto temporal dementia

Answer 65

• Selective serotonin reuptake inhibitors have shown effectiveness in treating some of the symptoms of frontotemporal dementia, especially compulsive behaviors.

Acetylcholinesterase inhibitors (donepezil, rivastigmine, and galantamine) and NMDA receptor antagonists (memantine) are not FDA approved for the treat- ment of frontotemporal dementia and have little evidence of benefit.

Question 66

Thymectomy in myasthenia gravis

Answer 66

• Indications for thymectomy in myasthenia gravis include the presence of thymoma and the need to minimize immunotherapy requirements in patients without thymoma who have active disease and positivity for acetylcholine receptor antibodies, are younger than 65 years, and are within 3 years of diagnosis

Question 67

MS vs NMO

Answer 67

Although NMO may present with symptoms that are similar to multiple sclerosis, distinguishing features include bilateral (rather than unilateral) optic neuritis and
longitudinally extensive (rather than segmental) myelitis.

If there is brain involvement, brainstem or hypothalamic syndromes may be seen. However, the brain may not be involved,
The marked spinal fluid pleocytosis with mostly neutrophils also is consistent with NMO and would be highly unusual for multiple sclerosis (MS) (in which cerebrospinal fluid [CSF] leukocytes are often normal or slightly elevated).

Aquaporin-4 antibody is a specific biomarker for NMO and has a direct role in the pathogenesis; diagnostic sensitivity and specificity has been reported to be as high as 91% and 100%, respectively.

Question 68

Intracranial hypotension

Answer 68

🔴Headache is the most common symptom of intracranial hypotension. 🔴Although this condition occurs most frequently after lumbar puncture, it can develop spontaneously.
🔴Headache presentation may be orthostatic, thunderclap, or subacute in nature. As with post-lumbar puncture headache, associated symptoms may include tinnitus, diplopia, neck pain, nausea, photophobia, and phonophobia.
🔴Diagnosis can be confirmed by a cerebrospinal fluid (CSF) opening pressure of less than 60 mm H₂O, but lumbar puncture may introduce another site of potential CSF leakage.
🔴Most clinicians rely on the contrast- enhanced brain MRI finding of diffuse nonnodular pachy- meningeal enhancement, which is seen in nearly 80% of affected patients. Cerebellar tonsillar descent, subdural fluid collections, decreased ventricular size, and engorgement of the pituitary gland are other common findings.
🔴Leaks typically are spinal, with precise site detection made in only 50% of patients by MRI or CT myelography. 🔴Those without identifiable sites are empirically treated with “blind” lumbar epidural blood patch (EBP) procedures, 🔴those with definable locations receive “targeted” EBP procedures at the appropriate site.

Question 69

Treatment of MS Flare

Answer 69

• The first-line treatment for multiple sclerosis relapses is high-dose glucocorticoids, typically administered as intravenous methylprednisolone (1 g/d for 3 to 5 days).

• Intramuscular adrenocorticotropin hormone gel and plasmapheresis are typically reserved as second-line treatments for multiple sclerosis relapses refractory to glucocorticoid treatment.

Question 70

AEDs in pregnancy

Answer 70

• In a woman with childbearing potential, lamotrigine and levetiracetam are the safest antiepileptic drug options.

Question 71

GBS treatment

Answer 71

Guillain-Barré syndrome is an acute autoimmune demyelinating polyradiculoneuropathy that presents with rapidly progressive flaccid weakness.

Plasma exchange and intravenous immunoglobulin are equally effective treatment options for Guillain- Barré syndrome.
Glucocorticoids are contraindicated in Guillain-Barré syndrome and may worsen outcome.

Question 72

Essential tremor management

Answer 72

• First-line pharmacologic treatments for essential tremor include propranolol, primidone, and topiramate.

• Surgical therapies, including deep-brain stimulation and focused ultrasound thalamotomy, can control tremor in refractory essential tremor associated with functional disability.

Question 73

Myoclonus vs dystonia

Answer 73

• Myoclonus is characterized by brief, shock-like, and jerky contractions that may originate from any part of the nervous system.

Dystonia can be differentiated from myoclonus on the basis of slow and sustained muscle contractions.

Question 74

TIA workup

Answer 74

The best diagnostic test for a patient who reports having an episode of painless, complete transient monocular vision loss consistent with a transient ischemic attack is carotid Doppler ultrasound to evaluate for significant extracranial carotid artery disease.

Question 75

Management of Duchene muscular dystrophy

Answer 75

Management of muscular dystrophy focuses on symptomatic therapy and supportive care. The American Academy of Neurology recommends offering low-dose prednisone (0.75 mg/kg/day) or deflazacort (0.9 mg/kg/day) to patients with Duchenne muscular dystrophy to improve strength and pulmonary function