Neurology - Jones Tower Flashcards
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.