Neurology - Jones Tower Flashcards
(21 cards)
Diagnose and manage nonconvulsive status epilepticus.
stat electroencephalography is the best next step in management to help confirm or rule out nonconvulsive status epilepticus.
Once electroencephalography has been performed, it may be necessary to pursue additional diagnostic studies as indicated, including brain MRI with contrast or lumbar puncture
status epilepticus is defined as
5 minutes or more of (1) continuous clinical and/or electrographic seizure activity or
(2) recurrent seizure activity without recovery (returning to baseline) between seizures
first-line treatment for status epilepticus
Benzodiazepines followed by urgent control therapy
intravenous fosphenytoin/phenytoin, valproate sodium, phenobarbital, levetiracetam, or continuous infusion midazolam. Patients remain on continuous electroencephalography during this process to ensure electrographic resolution of nonconvulsive status epilepticus.
Guide the appropriate workup for transient ischemic attack.
Admit the patient for brain MRI, vessel imaging, telemetry monitoring, and echocardiography
The ABCD2 score is calculated as follows: in TIA
A: age ≥60 years (1 point)
B: systolic blood pressure >140 mm Hg and/or diastolic blood pressure >90 mm Hg (1 point)
C: clinical features; speech disturbance without focal weakness (1 point); unilateral weakness (2 points)
D: duration of symptoms; 10-59 minutes (1 point); ≥60 minutes (2 points)
D: diabetes mellitus (1 point)
Transient ischemic attacks (TIAs) are
brief episodes of neurologic dysfunction resulting from focal cerebral ischemia not associated with permanent cerebral infarction
pseudotumor cerebri syndrome (PTCS)
disorders that cause elevated intracranial pressure without an intracranial mass, infection, or malignancy. Headache is the most frequent symptom, and while it is an uncommon disorder, it has an increased prevalence among obese women of childbearing age. PTCS-related headaches are typically bifrontal or retro-orbital, occur daily, and are progressive,
Diagnosis of PTCS
presence of papilledema, enlarged blind spot, visual field defect, sixth nerve palsy, and/or increased cerebrospinal fluid pressure greater than 200 mm H20 as assessed by lumbar puncture, with normal cerebrospinal fluid chemistry.
Treatments available for PTCS include removal of cerebrospinal fluid by lumbar puncture, acetazolamide (Answer B), and weight loss
effective migraine management
abortive therapy to be initiated as soon as possible at symptom onset. The most common treatment is triptans if not tolerated, ergot-derivatives may be used.
Manage patients with acute subdural hematoma
Generally, if a patient with subdural hematoma does not show signs of deteriorating neurologic deficits, hematoma size is not too large (approximately <10 mm), or midline shift is less than 5 mm, no emergent surgical intervention is necessary and the patient can be managed symptomatically
a known and life-threatening complication of subarachnoid hemorrhage,
transcranial ultrasonography can be used to detect development of vasospasm, Tx with Nimodipine
acute subdural hematoma require monitoring for the development of increased intracranial pressure?
eg, worsening headache, confusion or obtundation, diplopia, or signs of herniation). In these circumstances, patients may need to be intubated and hypertonic saline initiated with close monitoring in the neurocritical care unit
Manage acute subarachnoid hemorrhage
treatment of high blood pressure with antihypertensive medication is recommended to prevent ischemic stroke, intracerebral hemorrhage, and cardiac, renal, and other end-organ injury (class I; level of evidence A). Pain control is essential as well.
Nimodipine is a calcium-channel blocker that has been shown to improve outcomes in subarachnoid hemorrhage.
Vascular imaging (with CT angiography and/or conventional cerebral angiography) should be performed as early as possible, as it is necessary to rule out aneurysmal subarachnoid hemorrhage for definitive treatment, either with surgical clipping or endovascular coiling. Therefore, cerebral angiography and blood pressure control with oral nimodipine is the best management
Identify vitamin B12 deficiency as a cause of progressive neurocognitive dysfunction.
glossitis
peripheral smear will still show the classic megaloblastic anemia with hypersegmented neutrophils
Vitamin B12 levels are low in most cases; if the vitamin B12 is borderline low, then the findings of elevated methylmalonic acid or plasma total homocysteine would support a diagnosis of vitamin B12 deficiency
Diagnose symmetric ascending paralysis with preserved sensation as consistent with acute inflammatory demyelinating polyneuropathy (Guillain-Barre syndrome).
The hallmark of acute inflammatory demyelinating polyneuropathy is a progressive, symmetric, ascending motor weakness with absent or reduced deep tendon reflexes
typically preceded by an infection that triggers autoimmune injury in peripheral nerve myelin, resulting in demyelination at the level of nerve roots.
Elevated cerebrospinal fluid protein with a normal cerebrospinal fluid leukocyte count is typically documented, and electromyography shows abnormalities consistent with demyelination at the nerve root level.
Intravenous immunoglobulin or plasma exchange effectively reduces the time to recovery and increases the amount of recoverable weakness in patients with Guillain-Barre syndrome/acute inflammatory demyelinating polyneuropathy and is the recommended treatment.
Identify which antiseizure medications are more suitable for elderly patients
With more than one seizure episode and the finding of a structural change in brain imaging, treatment with an antiseizure medication is indicated to reduce the risk of recurrent seizures.
Lamotrigine is well tolerated by most elderly patients and is generally safe in those with kidney disease. Rash is the most common adverse effect
Oxcarbazepine/triliptal
associated with hyponatremia
Order the most appropriate diagnostic tests in a stable patient with new-onset seizures
first step in evaluating a stable patient who has experienced a first seizure is to check for structural brain abnormalities as the underlying cause.
Head MRI is superior to CT n this regard, and it is the best diagnostic test to perform now.
Head CT would be preferred if the patient were acutely sick or if stroke were suspected to rule out hemorrhagic stroke before thrombolytic therapy is considered.
Recommend treatment for Bell palsy.
The mainstay of treatment of Bell palsy involves corticosteroid therapy within 72 hours of symptom onset. The recommended initial prednisone dosage is 60 mg daily for 5 days followed by a 5-day taper. In cases of moderate to severe weakness (House-Brackmann grade IV or above), the addition of antiviral agents (valacyclovir 1000 mg 3 times daily for 5 days) may offer modest benefit in combination with corticosteroids
In addition to medical management, protecting the eye is imperative, especially in severe cases in which the patient is at risk for corneal injury. Artificial tears should be applied every hour while awake and ointment formulation and patches can be used at night. Protective glasses or goggles should be prescribed.
Bell palsy
Affected patients usually present with sudden onset (over a few hours to days) unilateral facial paralysis. Symptoms typically progress within the first 3 weeks and then improve within 6 months
an acute peripheral facial nerve palsy of unknown cause and it accounts for about one-half of all cases of facial nerve palsies. Although Bell palsy has no predilection for age, sex, or geographic location, the risk is 3 times greater in pregnancy, specifically in the third trimester and early postpartum (first week), and 5% to 10% of all patients who develop Bell palsy have diabetes mellitus. Bell palsy is thought to be most commonly due to activation of the herpes simplex virus, although other infectious agents include herpes zoster, cytomegalovirus, Epstein-Barr virus, adenovirus, influenza B, and coxsackievirus.
Manage asymptomatic, incidental intracranial aneurysm.
outpatient follow-up would be appropriate. A suggested follow-up regimen is to repeat imaging (CT or MR angiography) in 6 to 12 months and then annually for 2 to 3 years.
If the aneurysm growth is stable thereafter, follow-up appointments can be arranged less frequently. Conventional cerebral angiography is an invasive procedure and is associated with more complications than CT or MR angiography and would not be indicated if noninvasive imaging already detected an aneurysm.
It can be performed when clinical suspicion for intracranial aneurysm is high and noninvasive imaging is negative.
