Approach to the Patient with Seizures



Approach to the Patient with Seizures


Vicenta Salanova



A. Seizures result from the paroxysmal, hypersynchronous, abnormal activity of neurons in the cerebral cortex. Seizures are common symptoms and can be manifestations of toxic-metabolic abnormalities or of infection, can be secondary to a variety of disorders that affect neuronal function, or can be idiopathic with unknown cause.

1. Nonrecurrent seizures—for example, toxic-metabolic, hypoxia.

2. Recurrent seizures or epilepsy—inherited, acquired, or structural cortical lesions.

B. The international classification of epileptic seizures consists of two main categories— partial seizures and generalized seizures.

1. Partial seizures (focal) result from localized epileptogenic lesions, except in children with benign focal epilepsy, who have no structural lesions. Partial seizures are subdivided as follows:



  • Simple partial seizures if there is preservation of consciousness.


  • Complex partial seizures if there is impairment of consciousness. A partial seizure typically begins as a simple partial seizure consisting of an aura reflecting the site of seizure origin (or ictal spread to the symptomatogenic area) and then evolves into a complex partial seizure. Both simple and complex partial seizures can evolve into secondarily generalized seizures.

2. Generalized seizures can be convulsive or nonconvulsive and are subdivided into absence (typical and atypical absences), myoclonic, clonic, tonic, tonic-clonic, and atonic seizures.

C. There is also an international classification of epilepsy and epilepsy syndromes. This classification takes into account the age at onset, possible etiologic factors, inheritance, findings at neurologic examination, prognosis, and seizure type (partial or generalized).

1. Localization-related epilepsy.



  • Idiopathic (benign childhood rolandic and occipital epilepsy).


  • Symptomatic, which is acquired and based mainly on the anatomic localization.

2. Generalized epilepsy and syndromes.



  • Idiopathic with age-related onset (e.g., benign neonatal familial convulsions, childhood and juvenile absence epilepsy, juvenile myoclonic epilepsy, and epilepsy with grand mal seizures on awakening).


  • Symptomatic (e.g., infantile spasms and Lennox-Gastaut’s syndrome). The international classification includes two other categories: (1) epileptic syndromes with both focal and generalized seizures (e.g., acquired epileptic aphasia) and (2) special syndromes (e.g., febrile convulsions). This chapter reviews the etiology, clinical manifestations, evaluation, and differential diagnoses of some of these types of seizures with emphasis on patients with partial seizures.


I. ETIOLOGY


A. Toxic-metabolic.


1. Systemic illness.

Hypoglycemia, nonketotic hyperglycemia, hypoxia, hypocalcemia (in patients with or without a history of hypoparathyroidism), hyponatremia (inappropriate antidiuretic hormone syndrome and water intoxication), hypomagnesemia, uremia and hepatic failure, sickle-cell anemia, thrombotic thrombocytopenic purpura, Whipple’s disease.



2. Drugs and toxins.

Cocaine, amphetamines, phencyclidine, lidocaine, lead poisoning. Others can lower the seizure threshold and increase the risk of seizures usually among patients with other predisposing factors (tricyclics, theophylline, phenothiazine, and penicillins).


3. Withdrawal syndromes.

Alcohol, hypnotics.

4. Pyridoxine deficiency.


B. Acquired structural lesions.


1. Infection.

Brain abscess, meningitis, encephalitis (e.g., herpes simplex encephalitis), postinfectious encephalomyelitis, cysticercosis, opportunistic infections in AIDS, neurosyphilis.


2. Vascular.

Vasculitis (systemic lupus erythematosus, hypersensitivity, and infectious vasculitis), ischemic or hemorrhagic cerebrovascular disease, cerebral venous thrombosis, arteriovenous malformation, cavernous angioma.


3. Trauma.

Usually penetrating, subdural hematoma.


4. Neoplasms

and other lesions. Primary or metastatic tumors, hamartomas, cortical dysplasia.


5. Mesial temporal sclerosis.

Usually postfebrile convulsions.


6. Other.

Alzheimer’s disease, Creutzfeldt-Jakob’s disease, and in rare instances, multiple sclerosis.


C. Familial.

1. Primary generalized epilepsy.

2. Benign focal epilepsy of childhood.

3. Febrile convulsions.

4. Autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE).

5. Familial temporal lobe epilepsy (FTLE).


D. Other genetic syndromes

associated with seizures (tuberous sclerosis and neurofibromatosis), disorders of amino acid, lipid, and protein metabolism (e.g., phenylketonuria, maple syrup urine disease, and porphyria).


II. CLINICAL MANIFESTATIONS


A. Metabolic-toxic and hypoxic insults.

Patients with seizures attributable to metabolic or toxic causes have generalized tonic-clonic seizures, but focal seizures and epilepsia partialis continua can occur with nonketotic hyperglycemia. Posthypoxic coma usually causes multifocal myoclonus; however, periodic lateralized epileptiform discharges (PLEDs) may be seen, at times associated with focal motor seizures.


B. Meningitis and encephalitis

can cause either generalized or focal seizures with secondarily generalized seizures. Patients with herpes simplex encephalitis often have complex partial seizures typical of those of temporal lobe origin. The EEG shows focal slowing in one or both temporal regions and PLEDs. MRI shows hypodense lesions in one or both temporal lobes.


C. Partial seizures

(functional-anatomic classification of epilepsy). Clinical features and EEG findings indicate focal origin.

1. Temporal lobe seizures are the most common partial seizures. In 30% of these patients, the seizures are refractory to medical treatment.



  • Signs and symptoms. The findings at neurologic examination often are normal, except for memory dysfunction, which can be seen in patients with bitemporal epilepsy. Most of these patients have an epigastric aura (nausea, an epigastric rising sensation, stomach upset, or even pain). Other aurae consist of fear, complex visual or auditory hallucinations, déjà vu, and olfactory and gustatory sensations. The clinical manifestations are stereotypical, and most patients have one seizure type. Most patients exhibit staring, unresponsiveness, and oroalimentary and gestural automatism. Some patients also have contralateral arm dystonic posturing. Ictal or postictal language difficulties also have lateralizing value. Ictal speech occurs in patients with seizures arising from the nondominant temporal lobe. Patients with seizures originating from the dominant temporal lobe may exhibit ictal and postictal dysphasia.



  • Etiologic factors and pathologic features. Mesial temporal sclerosis is the most common pathologic finding. There is a strong association between mesial temporal sclerosis and prolonged complex febrile seizures in patients younger than 5 years of age. There usually is a silent interval between the occurrence of febrile seizures and the onset of mesial temporal lobe epilepsy, which often begins toward the end of the first decade of life or soon after. Other pathologic findings include tumors such as ganglioglioma, cortical dysplasia, and cavernous malformation. As many as 15% of patients with medically refractory temporal lobe epilepsy have evidence of a dual pathologic process. Mesial temporal sclerosis can occur with temporal lobe developmental lesions such as cortical dysplasia and subependymal heterotopia.


  • EEG findings include epileptiform discharges over the anterior temporal region and often polymorphic slowing. About 30% to 40% of these patients have bitemporal independent interictal epileptiform discharges, usually with predominance on the side of ictal onset.


  • Imaging studies. MRI volumetric studies usually show a smaller hippocampus and increased signal intensity on T2-weighted images that are indicative of hippocampal sclerosis. These changes can be seen in as many as 80% of patients with refractory temporal lobe epilepsy.


  • Secondarily generalized tonic-clonic seizures and convulsive status epilepticus can occur; nonconvulsive complex partial status epilepticus is rare.


  • Patients with temporal lobe seizures should be differentiated from patients with FTLE. The first series described FTLE as a benign disorder with late age of onset, excellent outcome, and normal finding on the MRI of the head. A second report, however, showed that some cases of FTLE were refractory to medical treatment, requiring surgical treatment. The most recent report concluded that FTLE is a clinically heterogeneous syndrome. The authors found hippocampal atrophy in 57% of their patients, including those with a benign course or remission of seizures. They concluded that the findings indicated the presence of a strong genetic component in the development of mesial temporal sclerosis in the families studied.

2. Focal motor seizures. These seizures originate in the vicinity of the rolandic motor cortex. Consciousness is preserved.



  • Signs and symptoms. Examination may show contralateral mild hemiparesis or hyperreflexia. Seizures commonly begin with focal contralateral twitching of the face or hand and then spread to involve the rest of the extremity. When seizures originate in the nondominant hemisphere, patients usually are able to speak during the seizures. When seizures originate in the dominant hemisphere, patients may have ictal and postictal aphasia. Clonic eye movements, blinking, and conscious contraversion also may occur. Ictal focal motor manifestations, postictal hemiparesis, and postictal aphasia are contralateral to the side of seizure onset. Some patients have continuous focal motor activity (epilepsia partialis continua lasting weeks, months, or even years).


  • Imaging studies. Focal structural lesions are common.


  • EEG shows focal slowing and focal epileptiform discharges over the frontal lobe; however, some patients have no epileptiform discharges on scalp recordings or have bifrontal epileptiform abnormalities.


  • Patients with focal motor seizures have to be differentiated from patients with benign rolandic epilepsy with centrotemporal spikes, which begins between the ages of 3 and 13 years. These children have normal findings at neurologic examination and imaging studies. They have nocturnal generalized seizures and partial seizures beginning in the face with preservation of consciousness, at times with speech arrest. The EEG shows centrotemporal, high-amplitude, broad, sharp waves and slow discharges, with a horizontal dipole, occurring predominantly during sleep. The prognosis is excellent.

3. Supplementary motor seizures originate in the supplementary motor cortex, which is located in the mesial frontal lobe anterior to the primary motor leg area.



  • Signs and symptoms. Findings at examination usually are normal. Almost one-half of these patients have a somatosensory aura consisting of tingling or numbness of
    the extremities, which can be contralateral or bilateral. These patients have unilateral or bilateral tonic posturing of the extremities at onset, vocalization, speech arrest, and laughter. Other manifestations include fencing posture, thrashing, kicking, and pelvic movements. Responsiveness is preserved unless the seizure evolves into a secondarily generalized tonic-clonic seizure. Supplementary motor seizures are common during sleep and are of short duration without postictal confusion or amnesia.


  • Imaging studies. MRI of the head may show lesions in the supplementary motor area.


  • The EEG may show epileptiform discharges over the vertex, but some patients may have no interictal epileptiform discharges on scalp recordings. Ictal recordings often are nonlateralized. A few patients may have no ictal EEG changes during scalp recordings.

4. Complex partial seizures of frontal lobe origin.

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Aug 18, 2016 | Posted by in NEUROLOGY | Comments Off on Approach to the Patient with Seizures

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