Partial Epilepsies Clinical Presentation

Obtaining a description of the seizures from the patient and any witnesses is critical. The description needs to include a description of the patient’s state of consciousness during the seizure. Consciousness usually is assessed by the ability of the patient to respond to external stimuli (ie, responsiveness).

Partial seizures are divided into simple, complex, and those that evolve into secondary generalized seizures. Simple and complex seizures are distinguished solely on the basis of the state of consciousness. This is intact in simple partial seizures and impaired in complex partial seizures.

Simple partial seizures

Simple partial seizures are subdivided into 4 categories, according to whether the symptoms are motor, sensory, autonomic, or psychic.

Motor symptoms can vary. They may include motor signs with or without march, versive movements, posturing, and phonatory symptoms.

Sensory symptoms include all 5 senses and a vertiginous sensation. With the exception of vertigo, these usually are characterized by elementary hallucinations.

Autonomic symptoms include the common rising epigastric sensation (typically observed in mesial temporal lobe epilepsy). Less frequent symptoms are vasomotor phenomena and mydriasis.

Psychic symptoms are characterized by various experiences involving memory (déjà-vu, jamais-vu), affect (fear, pleasure), or other complex psychic phenomena such as illusions.

Complex partial seizures

Complex partial seizures include some complex symptomatology (ie, automatisms) and, by definition, an impairment of consciousness. Automatisms consist of involuntary but coordinated motor activity, which tends to be purposeless and repetitive. Common automatisms include lip smacking, chewing, fidgeting, and walking.

Complex partial seizures can begin as simple partial seizures and seizures with impaired consciousness at onset. Complex partial seizures are not subdivided according to coexisting symptoms, no matter how prominent.

Partial seizures that evolve into generalized seizures

The third type of partial seizure evolves into a generalized seizure. This is divided further according to what precedes generalization (simple partial seizure only, complex partial seizure only, simple partial seizure evolving into complex partial seizure). For clinical purposes, however, the partial phase of the seizure often is missed and many patients simply present with a convulsion (secondarily generalized tonic-clonic seizures).

Genetic partial epilepsies

Three genetic partial epilepsies are recognized, as follows:

• Childhood epilepsy of occipital paroxysms
• Benign childhood epilepsy with centrotemporal spikes
• Autosomal dominant nocturnal frontal lobe epilepsy

Childhood epilepsy of occipital paroxysms

Age of onset is 15 months to 17 years. One third of patients have a family history of epilepsy, especially rolandic epilepsy.

Symptoms of attacks include the following:

• Visual hallucination
• Blindness
• Hemianopia
• Visual illusions (eg, micropsia, macropsia, metamorphopsia)
• Loss of consciousness
• Unilateral clonic seizure followed by migraine like headache

These attacks can occur while the child is awake or sleeping. They tend to occur during the transition period between wakefulness and sleep.

Benign childhood epilepsy with centrotemporal spikes

Age of onset is 2-12 years, with a strong peak at 8-9 years.

Characteristic ictal symptoms include the following:

• Guttural vocalizations
• Hypersalivation
• Drooling
• Sensations or movements of the mouth
• Dysphasia
• Speech arrest

Though these focal seizures are the most characteristic seizure types, they can be quite subtle and are missed easily. The most common mode of presentation is a nocturnal (secondary) generalized tonic-clonic seizure during sleep.

Neurologic examination is normal. The natural history is benign. This syndrome has an excellent prognosis regardless of treatment, with spontaneous remission by age 14-16 years. If treatment is required, options may include carbamazepine, gabapentin, or valproate. Antiepileptic drugs (AEDs) should always be weaned by age 14-16 years.

Autosomal dominant nocturnal frontal lobe epilepsy

Autosomal dominant nocturnal (ADNFLE) is a recently described syndrome. Onset is early in life.

ADNFLE is caused by mutation in the neuronal nicotinic acetylcholine receptor alpha4 subunit (CHRNA4) gene. Several mutations of this gene have been identified as causes of ADNFLE. Despite its established genetic basis, the genetic findings are variable (locus heterogeneity); thus, definite diagnosis is difficult and largely one of exclusion.

Seizures are nocturnal and occur in clusters, mimicking parasomnias. They mostly are brief tonic seizures and rare tonic-clonic convulsions, often preceded by a nonspecific aura.

Seizures often subside with age and may even disappear at adulthood. They usually are controlled with carbamazepine.

In most focal epilepsies, physical examination is unrevealing. A neurologic examination should be done to elicit any cortical abnormality or dysfunction, which would depend on etiology and lesion site.