ABPN Neurology key terms

Bundle of upper motor neuron axons running from the motor cortex to brainstem nuclei that control cranial muscles. Bilateral lesions produce pseudobulbar palsy with dysarthria, dysphagia, and emotional lability.

Topographic map of body parts along the precentral and postcentral gyri, with the leg represented medially near the longitudinal fissure and the face laterally. It explains stroke deficits that follow vascular territories.

Nonfluent speech output with relatively preserved comprehension and impaired repetition, caused by injury to the dominant inferior frontal gyrus. Patients often have right-sided weakness because the lesion involves adjacent motor cortex.

Inability to form new declarative memories after the causative event, with remote memories often spared. Bilateral medial temporal or diencephalic damage, as in Korsakoff syndrome, is a common cause.

Failure to attend to or act on one side of space, usually the left, after a right hemisphere lesion, most often right parietal or frontal. It differs from hemianopia because patients may see but not respond.

Physiologic mechanism that keeps cerebral blood flow nearly constant across a range of mean arterial pressures, roughly 60 to 150 mmHg in healthy adults. It fails in acute injury, making perfusion pressure critical.

Ischemic lesion at the boundary between two major arterial territories, typically from systemic hypotension. Damage is often bilateral and involves proximal limb weakness more than face or hand.

Occlusion of dural venous channels or cortical veins by thrombus, causing headache, seizures, and hemorrhagic infarction. Risk factors include pregnancy, estrogen use, thrombophilia, and dehydration.

Continuous seizure activity lasting five minutes or more, or repeated seizures without recovery between them. It is a medical emergency requiring immediate benzodiazepine, because prolonged seizures cause neuronal injury.

Posterior dominant 8 to 13 Hz sinusoidal activity seen in relaxed wakefulness with eyes closed, attenuating with eye opening. Its presence and reactivity help confirm normal cortical function and distinguish sleep or encephalopathy.

Repetitive sharp-contoured waveforms occurring at nearly regular intervals in one hemisphere, often with acute structural lesions such as stroke or herpes encephalitis, and frequently associated with nonconvulsive seizures.

Self-propagating wave of neuronal depolarization and depressed activity that moves slowly across cortex. It is the leading explanation for migraine aura and may activate trigeminal nociceptors.

Chronic daily headache worsened by frequent use of acute analgesics or triptans, typically 10 to 15 days per month. Treatment requires stopping the overused drug while starting preventive therapy.

Severe unilateral orbital or temporal pain with ipsilateral autonomic signs such as tearing and ptosis, lasting 15 to 180 minutes per attack. It is treated acutely with high-flow oxygen or triptans.

Brief electric-shock facial pain in one or more divisions of the trigeminal nerve, often triggered by touch, chewing, or cold. Most cases reflect vascular compression of the nerve root entry zone.

Summed electrical response of muscle fibers recorded over a muscle after supramaximal nerve stimulation. Its amplitude reflects the number of functioning axons and motor units.

Acute immune-mediated polyradiculoneuropathy causing progressive symmetric weakness, areflexia, and often autonomic instability. Albuminocytologic dissociation in cerebrospinal fluid and reduced response amplitudes support the diagnosis.

Life-threatening exacerbation of myasthenia gravis with respiratory muscle weakness requiring ventilation. Triggers include infection, surgery, and medication changes; treatment is plasma exchange or intravenous immunoglobulin.

Involuntary choreiform or dystonic movements that appear during the peak effect of levodopa in advanced Parkinson disease. They reflect pulsatile dopaminergic stimulation and often limit dose escalation.

Bilateral postural and action tremor of the hands, sometimes with head or voice involvement, without other neurologic deficits. It is distinguished from Parkinson tremor, which is typically rest-predominant and asymmetric.

Sustained or intermittent muscle contractions producing abnormal postures or twisting movements, often worsened by voluntary action. It can be focal, segmental, or generalized and may be genetic or acquired.

Immunoglobulin G bands present in cerebrospinal fluid but absent from matched serum, indicating intrathecal antibody synthesis. They support a diagnosis of multiple sclerosis but are not specific for it.

Autoimmune limbic encephalitis causing psychiatric symptoms, memory loss, seizures, dyskinesias, and autonomic instability, often with ovarian teratoma. Diagnosis requires antibody testing of cerebrospinal fluid.

Demyelinating disease of the brain caused by reactivation of JC virus in immunosuppressed patients, producing asymmetric white matter lesions and progressive deficits without mass effect or contrast enhancement.

Spread of cancer to the pia and arachnoid, causing headache, cranial neuropathies, radicular pain, and hydrocephalus. Cerebrospinal fluid cytology and contrast-enhanced magnetic resonance imaging are needed for diagnosis.

Apparent worsening of tumor or new enhancement on imaging shortly after chemoradiation, caused by treatment-related inflammation rather than true tumor growth. It usually improves without changing therapy.

Impaired adduction of one eye with abducting nystagmus in the other, caused by a lesion of the medial longitudinal fasciculus. In younger patients it suggests demyelinating disease; in older patients, brainstem ischemia.

Brief episodes of spinning triggered by changes in head position, caused by displaced otoconia in a semicircular canal. The Dix-Hallpike maneuver confirms it and canalith repositioning treats it.

Bilateral optic disc swelling from raised intracranial pressure, with preserved visual acuity early and enlarged blind spots. It signals a serious process such as mass lesion, venous thrombosis, or idiopathic intracranial hypertension.

Convulsion occurring between 6 months and 5 years of age with fever but no intracranial infection, in a child without prior afebrile seizures. Simple episodes are brief and generalized, with low recurrence risk.

Epileptic syndrome of infancy with clusters of flexor or extensor spasms and an electroencephalogram showing hypsarrhythmia. It requires urgent treatment because it causes developmental regression.

Nonprogressive disorder of movement and posture resulting from early brain injury, often perinatal. Spastic diplegia from periventricular leukomalacia and dyskinetic forms from basal ganglia damage are common patterns.

Blood collection between skull and dura, usually from middle meningeal artery injury with a temporal bone fracture. A lucid interval may precede rapid deterioration from uncal herniation.

Widespread shearing of white matter tracts from rotational acceleration-deceleration, causing immediate coma without a large mass lesion. Imaging may be normal early, and outcome depends on brainstem involvement.

Mean arterial pressure minus intracranial pressure; the driving pressure for cerebral blood flow. Targets near 60 to 70 mmHg are used after traumatic brain injury to avoid ischemia.

Thiamine deficiency producing acute confusion, ophthalmoplegia, and ataxia. It is a medical emergency treated with parenteral thiamine before glucose, and may progress to Korsakoff syndrome.

Noninflammatory demyelination of the pons and sometimes extrapontine structures after rapid correction of hyponatremia, causing dysarthria, dysphagia, quadriparesis, and locked-in syndrome. Prevention is slow sodium correction.

Hyperthermia, agitation, clonus, hyperreflexia, and autonomic instability from serotonergic drug excess or interaction. It is distinguished from neuroleptic malignant syndrome by prominent clonus and rapid onset.