Egyptian Board Neurology key terms

Breakdown of the axon and its myelin sheath distal to a nerve injury, followed by macrophage clearance and later remyelination. It explains why weakness and atrophy can worsen for days after acute axonal lesions.

Findings of corticospinal tract dysfunction: spasticity, hyperreflexia, extensor plantar response, and loss of fine dexterity, with little early atrophy. They localise disease above the anterior horn cell.

Findings of anterior horn cell, root, or peripheral nerve disease: flaccid weakness, atrophy, fasciculations, and reduced reflexes. They place the lesion in the motor unit rather than the corticospinal pathway.

Topographic map of the body on the precentral and postcentral gyri, with the leg represented medially in the interhemispheric fissure and the face laterally. It predicts deficit patterns in cortical stroke.

Intrinsic adjustment of arteriolar calibre that keeps cerebral blood flow near constant across a mean arterial pressure range of roughly 60 to 150 mmHg. It is impaired in acute injury and in chronic hypertension.

Mean arterial pressure minus intracranial pressure, normally about 70 to 90 mmHg. It drives cerebral blood flow and is the target of haemodynamic management after severe brain injury.

Glutamate-driven calcium influx and downstream enzyme activation that kills neurons after ischaemia, seizures, or trauma. It is the rationale for glutamate blockade research and for avoiding hyperthermia and hypoglycaemia in acute brain injury.

Posterior dominant 8 to 13 Hz rhythm seen with eyes closed and relaxed wakefulness, attenuating on eye opening. Its normal presence and reactivity are key markers of a healthy awake cerebral cortex.

Hyperventilation, intermittent photic stimulation, and sleep deprivation used to provoke epileptiform discharges or reveal abnormalities not present at rest. Each has characteristic normal responses and specific risks.

Spike, polyspike, sharp wave, or spike-and-wave complex that stands out from background and reflects hypersynchronous neuronal firing. It supports but does not by itself confirm a diagnosis of epilepsy.

Electrical stimulation of a nerve with recording of the compound muscle action potential or sensory nerve action potential to measure latency, amplitude, and conduction velocity. It distinguishes demyelinating from axonal pathology.

Recording of spontaneous and voluntary muscle electrical activity with a needle electrode, assessing fibrillation potentials, motor unit potential size, and recruitment. It localises lesions to nerve, root, plexus, or muscle.

Repeated supramaximal stimulation at 2 to 3 Hz to look for a decrement in compound muscle action potential amplitude, the hallmark of postsynaptic neuromuscular junction failure such as myasthenia gravis.

Cortical and spinal responses to peripheral nerve stimulation, used to assess central sensory pathway conduction and to help predict outcome in coma or spinal cord injury. Prolonged latencies suggest demyelination.

Hypoperfused but still viable brain tissue surrounding an infarct core, at risk of infarction but salvageable with timely reperfusion. Its presence on perfusion imaging guides thrombectomy and thrombolysis decisions.

Endovascular removal of a large vessel occlusion, most effective within 6 hours of onset and up to 24 hours in selected patients with favourable imaging. It is the standard of care for proximal anterior circulation occlusion.

Ten-point grading of early ischaemic change on non-contrast CT, subtracting one point per affected region from 10. Lower scores indicate larger established infarction and greater haemorrhage risk with reperfusion.

Bleeding into infarcted tissue after ischaemic stroke, ranging from petechial haemorrhage to space-occupying haematoma. Risk rises with large infarcts, thrombolysis, anticoagulation, and uncontrolled hypertension.

Bleeding within brain parenchyma, usually from small vessel disease or hypertension, presenting with acute headache, vomiting, and focal deficit. Management prioritises blood pressure control, reversal of anticoagulation, and neurosurgical assessment.

Bleeding into the subarachnoid space, typically from a ruptured saccular aneurysm, causing thunderclap headache, meningism, and risk of vasospasm and hydrocephalus. CT and lumbar puncture establish the diagnosis.

Neurological deterioration from vasospasm and other mechanisms between days 3 and 14 after subarachnoid haemorrhage. Nimodipine and euvolaemic management reduce its impact; surveillance uses transcranial Doppler and clinical monitoring.

Thrombosis of dural sinuses or cortical veins causing headache, papilloedema, seizures, and venous infarction that may haemorrhage. Diagnosis requires venous imaging; anticoagulation is given even when haemorrhage is present.

Continuous seizure activity or repeated seizures without recovery lasting 5 minutes or more, requiring immediate benzodiazepine followed by a second-line antiseizure drug. Prolonged episodes cause excitotoxic injury and systemic complications.

A seizure beginning in one hemisphere that spreads to involve both, previously called secondary generalisation. The focal onset carries localising value and influences drug and surgical decisions.

Drug that reduces seizure occurrence by modulating sodium channels, GABA transmission, or synaptic vesicle release. Choice depends on seizure type, comorbidity, teratogenicity, and interaction profile rather than potency alone.

Reversible focal neurological symptoms, usually visual, developing over 5 to 20 minutes and lasting under 60 minutes before headache. It reflects cortical spreading depression and matters for stroke risk assessment.

Group of primary headaches with unilateral trigeminal pain and ipsilateral autonomic features such as lacrimation and ptosis, exemplified by cluster headache. Attacks are short and severe and respond to high-flow oxygen.

Paroxysmal electric-shock facial pain in one or more trigeminal divisions, often triggered by touch, chewing, or cold. Carbamazepine is first line, and neurovascular conflict warrants imaging.

Chronic daily headache perpetuated by frequent use of acute analgesics or triptans, typically over 10 to 15 days per month. Treatment requires withdrawal of the overused drug plus prophylaxis.

Peripheral nerve disorder affecting axons primarily, producing length-dependent sensory loss and weakness with reduced amplitudes but preserved conduction velocities. Diabetes and toxic exposures are common causes.

Autoimmune postsynaptic neuromuscular junction disorder causing fatigable ptosis, diplopia, bulbar and limb weakness, often with acetylcholine receptor antibodies and thymic abnormality. Crisis with respiratory failure is the key emergency.

Presynaptic neuromuscular junction disorder with antibodies to voltage-gated calcium channels, causing proximal weakness that improves with use and often accompanies small cell lung cancer. Reflexes are reduced and incremental response occurs on high-frequency stimulation.

Progressive motor neuron degeneration combining upper and lower motor neuron signs in multiple regions without sensory loss. Diagnosis is clinical with supportive electromyography, and riluzole or edaravone offer modest benefit.

Primary muscle disease causing proximal weakness, normal or mildly raised creatine kinase, and myopathic electromyography with short small motor unit potentials. Inflammatory, metabolic, and genetic forms require different workup.

Diagnostic framework for multiple sclerosis requiring dissemination of demyelinating lesions in space and time, supported by MRI, cerebrospinal fluid oligoclonal bands, and evoked potentials. It allows diagnosis after a first attack in many patients.

Restricted immunoglobulin G bands in cerebrospinal fluid absent from paired serum, indicating intrathecal synthesis. They support multiple sclerosis diagnosis but also occur in infection and other inflammatory disease.

Astrocytopathy caused by aquaporin-4 antibodies, producing optic neuritis, longitudinally extensive myelitis, and area postrema syndrome. Attacks are severe and require acute plasma exchange plus long-term immunosuppression.

Central nervous system infection by Mycobacterium tuberculosis, most often basal meningitis with hydrocephalus, cranial nerve palsy, and tuberculoma. Diagnosis relies on cerebrospinal fluid analysis and imaging; treatment is prolonged multidrug therapy with steroids in meningitis.

Spectrum of cognitive impairment in HIV infection ranging from asymptomatic deficits to disabling dementia, driven by viral and inflammatory mechanisms. Effective antiretroviral therapy is central, with attention to drug interactions.

Demyelinating brain infection by JC virus occurring in immunosuppression, producing asymmetric white matter lesions without mass effect. Restoration of immunity is the main treatment and carries risk of immune reconstitution inflammatory syndrome.

Elevation of pressure within the rigid skull from mass, oedema, or impaired cerebrospinal fluid flow, threatening herniation and perfusion. Headache, vomiting, papilloedema, and declining consciousness are warning signs.

Irreversible loss of all brain and brainstem function demonstrated by deep unresponsive coma, absent brainstem reflexes, and apnoea, with cause and confounders excluded. Ancillary testing such as EEG may be required by local protocol.

Summed eye, verbal, and motor scores from 3 to 15 quantifying level of consciousness after acute brain injury. It guides triage, monitoring, and communication but is limited by intubation and sedation.

Contrast-enhancing mass with a dark centre on CT or MRI, seen in abscess, tumour, tuberculoma, and demyelination. Clinical context, diffusion restriction, and spectroscopy help distinguish these causes.

Spread of cancer to the pia and arachnoid, causing headache, cranial neuropathies, and radicular symptoms with malignant cells in cerebrospinal fluid. MRI with contrast and cerebrospinal fluid cytology confirm it.

Immune-mediated neurological dysfunction triggered by cancer, often presenting before the tumour is found and associated with specific antibodies. Recognition prompts cancer screening and early immunotherapy.