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Treat new convulsions during labour as possible eclampsia: protect breathing, terminate and prevent seizures, control severe hypertension, and plan birth after stabilisation. Previous good health does not exclude pre-eclampsia or eclampsia. Also consider epilepsy, hypoglycaemia, intracranial disease and other causes if the clinical findings suggest them; neither an invented history nor a fabricated urine result is needed to recognise the emergency.

Summon obstetric, anaesthetic and neonatal assistance. Protect the woman from injury, position her safely on her side when feasible, maintain the airway, and assess breathing and oxygen saturation. Do not force an object into her mouth or attempt to suppress a fit by forcefully holding down her limbs. Obtain intravenous access, check blood glucose, and measure blood pressure; assess platelets, renal function, liver tests and proteinuria without delaying essential treatment. Review the fetal condition once maternal resuscitation is under way.

Current first-line anticonvulsant treatment is magnesium sulfate. NICE describes an intravenous loading dose of 4 g over 5–15 minutes, followed by 1 g per hour, with continued treatment for 24 hours after the last fit. Recurrent fits require additional treatment under the emergency protocol. Monitor breathing, tendon reflexes and urine output because impaired renal function increases the risk of magnesium accumulation. A benzodiazepine is not an interchangeable routine substitute for magnesium sulfate in this setting. Severe hypertension requires prompt suitable treatment, for example labetalol, nifedipine or hydralazine, with continuing reassessment.^[ref]

Once stabilised, the woman needs a plan for birth. Cervical findings, progress of labour, gestation and maternal and fetal condition determine whether vaginal birth or Caesarean section is appropriate. Performing an immediate instrumental delivery during an uncontrolled fit is not a general rule, nor does the occurrence of one fit automatically establish the route of birth. Observation and treatment continue after delivery because further fits in eclampsia can occur.^[ref]

Historically, bloodletting, purgation, chloroform and expedited delivery were advocated in different combinations. An actual 1864 case report records such treatment and continuing convulsions despite delivery. It illustrates the historical problem, not proof that removal of blood or pressure on pelvic nerves explains or cures eclampsia.^[ref] Modern eclampsia care replaces those obsolete theories with specific seizure treatment, blood-pressure control and maternal resuscitation.

Discuss paralysis and convulsions separately: both historical labels describe manifestations with several causes. Their occurrence in infancy does not establish one diagnosis, and neither permits invention of examination findings absent from the paper.

For infantile paralysis, distinguish an acute loss of movement after an illness from impaired movement present from birth, delayed motor development and progressive weakness. Note distribution, muscle tone, tendon reflexes, sensation, pain, muscle atrophy, and bulbar or respiratory involvement. The classic acute flaccid, often asymmetric syndrome later identified with poliomyelitis must be distinguished from cerebral injury, cerebral palsy, peripheral nerve injury, spinal disease and painful failure to move a limb. A child who avoids movement because it hurts has pseudoparalysis, not necessarily loss of motor innervation.

An 1866 explanation might attribute some cases to teething, chill or constitutional weakness, and use rubbing, warmth, supports or electrical stimulation. Such attributions need qualification: a preceding event does not prove the mechanism, and electrical contraction does not demonstrate restoration of damaged motor neurons. The clinically useful period aims were preservation of comfort, nutrition and limb position and prevention of deformity while following recovery. No historical stimulant can be assumed to regenerate destroyed neural tissue.

Modern correction: acute weakness requires urgent localization and evaluation of breathing and swallowing. Poliomyelitis results from poliovirus infection and can permanently damage motor function; there is no specific curative treatment for paralytic disease. Supportive care and appropriate rehabilitation address respiratory risk, function and complications; vaccination is preventive rather than a reversal of established paralysis.^[ref] Cerebral palsy describes a different developmental motor disorder associated with disturbances of the developing brain; assessment, investigation when appropriate, physiotherapy, occupational support and treatment of associated problems are individualized. Not every case is attributable to a single event during delivery, and loss of previously attained abilities requires reconsideration of a static diagnosis.^[ref]

For infantile convulsions, consider fever, meningitis, encephalitis, hypoglycaemia, hypocalcaemia and other metabolic disorders, head injury, structural cerebral disease, toxic exposure and epilepsy. Clarify the age, duration, whether movements are focal, recovery between attacks and the child's condition before and afterwards. Neonatal seizures and convulsions in an older febrile infant should not be collapsed into one reassuring category. “Teething” is not a satisfactory explanation for a serious seizure, and a warm bath or gum-lancing must not replace investigation.

During an attack, protect the airway and prevent injury; do not put objects or oral medicines into the mouth. Assess breathing and circulation, time the event, check blood glucose promptly and identify reversible causes. A convulsive seizure lasting five minutes or more is a medical emergency requiring resuscitation and a current status epilepticus pathway, beginning with an appropriate benzodiazepine and escalating if needed. Hypoglycaemia, infection and electrolyte disturbances need direct treatment as well as suppression of movements.^[ref][ref] Following the event, investigate the cause and arrange appropriate follow-up; one provoked convulsion does not by itself establish chronic epilepsy.

There is no single constant anatomical lesion of epilepsy. A sound autopsy answer separates an underlying brain lesion, changes associated with longstanding epilepsy, and the consequences of the final seizure or death.

The potentially causal group includes healed traumatic scars, old cerebral infarctions or intracranial haemorrhages, developmental abnormalities of the cerebral cortex, brain tumours, and inflammatory or infectious destruction of brain tissue. Such abnormalities can leave an enduring network capable of generating recurrent seizures. Their importance depends on location and the lifetime history; an incidental abnormality is not automatically the cause. A modern acute symptomatic seizure during a transient metabolic disturbance should also not automatically be called epilepsy.^[ref]

In longstanding cases one may find atrophy or scarring of particular brain regions. Hippocampal sclerosis is an important modern example: loss of neurons with gliosis in the hippocampus, associated especially with temporal-lobe epilepsy. Association does not settle whether a particular lesion preceded the first seizure, resulted from repeated seizures, or shares another cause with them. Conversely, genetically determined disturbances of neuronal excitability can produce recurrent seizures without a grossly visible destructive lesion.^[ref]

For the historical question, vascular redness or congestion and alterations around the medulla oblongata deserve mention as contemporary observations rather than established universal causes. A January 1864 report describes microscopic examination of fourteen longstanding cases, including dilated blood vessels and altered nervous material in that region. Its proposed localization of epilepsy to the medulla oblongata is a historical theory; modern epilepsy is not defined by that site or by those vascular appearances.^[ref]

The terminal group includes cerebral oedema, hypoxic-ischaemic brain injury, and pulmonary oedema or aspiration in some deaths. Congestion is nonspecific and may be terminal; injuries can result from a fall during a seizure. None of these alone establishes that epilepsy was the original cause. A modern autopsy study of sudden deaths in people with epilepsy found both structural abnormalities and nonspecific changes; exclusion of another anatomical or toxicological cause remains central to classifying sudden unexpected death in epilepsy.^[ref]

The appropriate investigation is therefore inspection followed by systematic histology, especially of the cerebral cortex and hippocampus on both sides, interpreted alongside the recorded seizure history and examination of other organs. A normal-looking brain does not exclude epilepsy, and a congested one does not prove it.

The chief physiological routes are abrupt failure of blood circulation, failure of pulmonary ventilation or gas exchange, or catastrophic failure of the central control of those functions. Historical clinical accounts used labels such as syncope, asphyxia and medical coma in explaining deaths; these terms describe broad physiological failures rather than identifying the underlying diseases.^[ref] A brief faint or ordinary medical coma is not itself necessarily fatal.

In primary circulatory failure, effective delivery of blood to the brain stops. Modern examples include ventricular fibrillation, pulseless ventricular tachycardia, severe bradyarrhythmia and asystole. They may arise in coronary artery disease, after myocardial infarction, in cardiomyopathy, or from inherited cardiac ion channel disorders. An electrical cause may leave little distinctive gross evidence at autopsy. These modern mechanisms refine the broad historical description of cardiac syncope.^[ref]

Mechanical interruption of blood circulation gives another group: massive haemorrhage, rupture of an aortic aneurysm, cardiac tamponade, and large pulmonary embolism. The immediate deficit differs in each. Haemorrhage removes circulating volume; cardiac tamponade prevents adequate filling; pulmonary embolism obstructs flow through the pulmonary circulation. All can end with critically low cardiac output even if some electrical activity persists.^[ref]

Respiratory failure includes obstruction of the airway by a foreign body, laryngeal oedema or aspiration; drowning; and depression of breathing by drugs or major brainstem injury. Oxygen delivery then fails and secondary cardiac arrest follows. Carbon monoxide poisoning and cyanide poisoning illustrate related failure of oxygen transport or use: not every hypoxic death is caused by physical obstruction of an airway.^{[ref][ref][ref]}

A major intracranial haemorrhage or rapidly developing brain herniation can destroy or compress the pathways maintaining consciousness and breathing. A severe disturbance of electrolytes, especially potassium, may instead act directly on the heart's electrical function. A fatal seizure can involve respiratory and circulatory mechanisms; sudden unexpected death in epilepsy remains a diagnosis requiring exclusion of other causes, not merely recognition of a history of epilepsy.^[ref]

The practical distinction is between mode, immediate mechanism and underlying cause. For example, rupture of an aneurysm can cause haemorrhage, then circulatory failure, then irreversible hypoxic-ischaemic brain injury. A complete explanation identifies that chain. Inspection, histology, examination of the airway and heart, and appropriately interpreted toxicology may establish it; an unexplained sudden death cannot be assigned a precise cause from its suddenness alone.