USMLE Forum Archives - USMLE Step 3 - SEIZURES
SEIZURES
meduploader - 05-15-09 14:06
A seizure is a paroxysmal neurologic event caused by abnormal, synchronous discharges from populations of cortical neurons.
Epilepsy is a condition in which patients have unprovoked recurrent seizures. The key step in diagnosis and treatment is to determine whether the initial seizure activity is generalized or focal in onset.
1° Generalized Seizures
Selected subtypes are as follows:
Tonic-clonic (grand mal):
The most common generalized seizure type; typically seen in genetic epilepsy syndromes and in seizures arising from metabolic abnormalities (e.g., hyponatremia, alcohol withdrawal, medications, CNS infections).
Begin with stiffening of the extremities (tonic phase), often associated with a guttural cry from contraction of the expiratory muscles, followed by rhythmic clonic jerking of the extremities.
Associated urinary incontinence, tongue biting, and postictal confusion is typically found.
Myoclonic:
A myoclonic jerk is an abrupt, brief, single contraction of a muscle group that produces a quick contraction and movement. Myoclonic seizures are characterized by frequent but asynchronous, nonrhythmic multifocal myoclonic jerks. Myoclonic jerks are most commonly seen with metabolic derangements (especially uremia) and are usually not epileptic.
An important genetic cause of myoclonic seizures is juvenile myoclonic epilepsy; patients often have “staring spells” during childhood (brief alterations in consciousness often associated with eye blinking or
chewing movements) and subsequently develop both myoclonic and tonic-clonic seizures in adolescence. They also experience myoclonic jerks when entering into or emerging from sleep.
Atonic: The epilepsy type that can most resemble syncope clinically. Characterized by the abrupt loss of all muscle tone associated with a brief loss of consciousness. Primarily seen with inherited forms of childhood epilepsy.
Lennox-Gastault syndrome is characterized by seizures of multiple types, impaired cognitive function and slow spike and wave activity on EEG. It usually presents in childhood.
Focal (Partial) Seizures
Much more common than 1° generalized seizures, focal seizures originate from a small, discrete focal lesion within the brain that gives rise to abnormal synchronized neuronal discharges. This activity may then spread to involve other areas of the brain. Subtypes are as follows:
Simple partial seizures:
Focal seizures in which no alteration of consciousness is noted.
Initial symptoms depend on the location of the seizure focus and commonly include twitching/jerking of one side of the body (focal motor seizures) or sensations of strange smells or sounds.
Complex partial seizures:
Evolve from simple partial seizures as the initial focal seizure activity spreads to involve some but not all of both cerebral hemispheres. In fact, the stereotypical warning or aura that many patients report is simply the manifestation of the initial simple partial seizure.
As seizure activity spreads, patients develop an impairment of consciousness and behavioral arrest during which they display stereotypical behaviors known as automatisms (e.g., lip smacking, chewing,
pulling at clothes).
In contrast to simple partial seizures, complex partial seizures are associated with postictal confusion and lethargy.
Complex partial seizures with 2° generalization:
In many patients with prolonged complex partial seizures, seizure activity can ultimately spread to involve the entire cerebral cortex. The manifestation of the “2° generalization” of the initial focal seizure activity is usually generalized tonic-clonic activity.
Generalized seizures can thus be either 1° (generalized seizure activity at onset) or 2° (initial focal activity that spreads to involve the entire cortex).
Todd’s paralysis:
Patients with focal-onset seizures often have transient (minutes to hours) focal weakness or paralysis following seizure termination. This weakness usually involves the area of the body first affected by the
seizure, providing an important clue to the focus of seizure onset.
A patient with a generalized tonic-clonic seizure who is subsequently noted to have a postictal left hemiparesis likely had a focal-onset seizure that began in the right hemisphere and secondarily generalized.
Temporal lobe epilepsy: The most common cause of simple and complex partial seizures is temporal lobe pathology, most commonly 2° to abnormalities of the hippocampus. Hippocampal sclerosis/calcification is seen on imaging. The classic auras of odd smells, sounds, or tastes are associated
with temporal lobe epilepsy.
DIAGNOSIS
If the patient has a known seizure disorder (epileptic), check anticonvulsant levels—this is usually the only test that is needed. Because therapeutic anticonvulsant levels are variable, one dose may be toxic for one patient and therapeutic for another. Therefore, take the range given in laboratory reports as a general guideline.
If the patient history is unclear or if this is the patient's first seizure:
CBC, electrolytes (K disorders doesn’t cause seizure), blood glucose, LFTs, renal function tests, serum calcium, urinalysis
CT scan of the head (urgently)—to identify a structural lesion
MRI of the brain (laters) —with and without gadolinium (first without)
An important part of the workup of a patient with a first seizure
More sensitive than a CT scan in identifying structural changes, but not always practical (e.g., in an unstable patient)
EEG: if the initial stet of diagnostic tests doesn’t reveal the etiologyof the seizure, then the EEG is performed. The EEG shouldn’t be done first
Although the EEG is the most helpful diagnostic test in the diagnosis of a seizure disorder, an abnormal EEG pattern alone is not adequate for the diagnosis of seizures.
A normal EEG in a patient with a first seizure is associated with a lower risk of recurrence.
LP and blood cultures—if patient is febrile
Laboratory values to check immediately in an unfamiliar, seizing patient
Serum calcium, Serum sodium , Serum glucose or Accu-Chek , BUN
TREATMENT
For all seizures, ABCs take priority: secure airway and roll patient onto his side to prevent aspiration.
Patients with a history of seizures (epilepsy)
Seizures in these patients are usually due to noncompliance with anticonvulsant therapy. (Even one missed dose can result in subtherapeutic levels). Give a loading dose of the anticonvulsant medication, and continue the regular regimen as before.
These patients should be chronically managed by a neurologist. Treatment with one of the standard antiepileptic drugs provides adequate control in 70% of adult patients. In another 15% to 20%, a combination regimen controls seizures.
If seizures persist, increase the dosage of the first anticonvulsant until signs of toxicity appear. Add a second drug if the seizures cannot be controlled with the drug of first choice.
If the seizures are controlled, have the patient continue the medication for at least 2 years. If the patient remains seizure-free, taper the medication(s) cautiously. Confirm this decision with a lack of seizure activity on the EEG.
Long term Rx of fisrt time seizures
Chronic antiepileptic therapy is generally not indicated after single seizure. There are several exceptions however. Treat chronically after the first time seizure in the following circumstances.
Srong family history of seizure
Abnormal EEG
Status epilepticus that required benzodiazepines to stop the seizures.
For generalized tonic-clonic seizures and partial seizures
Phenytoin and carbamazepine are the drugs of choice. They are equally effective, and side-effect profiles are similar.
Other options include phenobarbital, valproate, and primidone.
For petit mal (absence) seizures—ethosuximide and valproic acid
Medications: Focal-onset seizures are best treated with anticonvulsants such as phenytoin, carbamazepine, phenobarbital, and valproic acid. Newer medications such as gabapentin, levetiracetam, lamotrigine, and topiramate are also useful.
Vagal nerve stimulators: Although their mechanism of action remains unclear, vagal nerve stimulators can ↓ the frequency of focal-onset seizures by 25% in patients with medically refractory seizures. A pacemaker-like device is implanted in the chest with leads attached to one of the vagal
nerves
Surgery: Patients with focal-onset seizures often have an identifiable brain lesion on imaging studies. This is particularly true of temporal lobe epilepsy 2° to hippocampal lesions. In such patients with medically refractory seizures, surgical resection of the causative lesion (e.g., temporal lobectomy) can produce striking results, with up to 50–75% of patients becoming seizure free.
Patients with epilepsy who fail to respond to three trials of antiepileptic drugs are unlikely to ever become seizure free with drug therapy. Treatment-resistant patients with epilepsy should be evaluated for a surgically remediable epilepsy syndrome.
Nonepileptic seizures of psychogenic origin can be differentiated from epilepsy by their longer duration, normal electroencephalogram findings, and maintenance of consciousness.
Nonepileptic psychogenic seizures are often associated with moaning, crying, and arrhythmic shaking of the body.
COMPLICATIONS
Anticonvulsants and OCPs: Drugs that induce the liver cytochrome P-450 system (e.g., phenytoin and carbamazepine) can lead to ↓ effective levels of other medications, including OCPs. All female patients taking such anticonvulsants should be counseled to consider other means of birth control or use OCPs with high levels of estrogen.
Zonisamide, valproic acid, tiagabine, levetiracetam, lamotrigine, gabapentin, and felbamate do not interfere with oral contraceptives.
Anticonvulsants and birth defects: Use of anticonvulsants during pregnancy is associated with an ↑ risk of birth defects, particularly neural tube defects. All women of childbearing age who use anticonvulsants should be advised to take at least 0.4 mg/day of folate. Pregnant women with epilepsy
should be treated with a single anticonvulsant at the lowest therapeutic dose; valproic acid is particularly teratogenic.
Prenatal diagnostic testing should be offered. In the third trimester, vitamin K, 10 mg daily, should be administered due to depression of clotting factor levels with many antiepileptics.
Elderly patients may be particularly sensitive to the cognitive, motor, and coordination side effects of phenytoin, even if the serum phenytoin level is in the therapeutic range. Gabapentin, lamotrigine, and carbamazepine are equally effective at controlling partial onset seizures in the elderly, but gabapentin and lamotrigine are better tolerated
Valproic acid, CBZ & gabapentin are all associated with weight gain
Lamotrigine is typically weight-neutral
Felbamate and Topiramate (SE: renal stones, confusion) are associated with weight loss.
meduploader - 05-15-09 14:06
A seizure is a paroxysmal neurologic event caused by abnormal, synchronous discharges from populations of cortical neurons.
Epilepsy is a condition in which patients have unprovoked recurrent seizures. The key step in diagnosis and treatment is to determine whether the initial seizure activity is generalized or focal in onset.
1° Generalized Seizures
Selected subtypes are as follows:
Tonic-clonic (grand mal):
The most common generalized seizure type; typically seen in genetic epilepsy syndromes and in seizures arising from metabolic abnormalities (e.g., hyponatremia, alcohol withdrawal, medications, CNS infections).
Begin with stiffening of the extremities (tonic phase), often associated with a guttural cry from contraction of the expiratory muscles, followed by rhythmic clonic jerking of the extremities.
Associated urinary incontinence, tongue biting, and postictal confusion is typically found.
Myoclonic:
A myoclonic jerk is an abrupt, brief, single contraction of a muscle group that produces a quick contraction and movement. Myoclonic seizures are characterized by frequent but asynchronous, nonrhythmic multifocal myoclonic jerks. Myoclonic jerks are most commonly seen with metabolic derangements (especially uremia) and are usually not epileptic.
An important genetic cause of myoclonic seizures is juvenile myoclonic epilepsy; patients often have “staring spells” during childhood (brief alterations in consciousness often associated with eye blinking or
chewing movements) and subsequently develop both myoclonic and tonic-clonic seizures in adolescence. They also experience myoclonic jerks when entering into or emerging from sleep.
Atonic: The epilepsy type that can most resemble syncope clinically. Characterized by the abrupt loss of all muscle tone associated with a brief loss of consciousness. Primarily seen with inherited forms of childhood epilepsy.
Lennox-Gastault syndrome is characterized by seizures of multiple types, impaired cognitive function and slow spike and wave activity on EEG. It usually presents in childhood.
Focal (Partial) Seizures
Much more common than 1° generalized seizures, focal seizures originate from a small, discrete focal lesion within the brain that gives rise to abnormal synchronized neuronal discharges. This activity may then spread to involve other areas of the brain. Subtypes are as follows:
Simple partial seizures:
Focal seizures in which no alteration of consciousness is noted.
Initial symptoms depend on the location of the seizure focus and commonly include twitching/jerking of one side of the body (focal motor seizures) or sensations of strange smells or sounds.
Complex partial seizures:
Evolve from simple partial seizures as the initial focal seizure activity spreads to involve some but not all of both cerebral hemispheres. In fact, the stereotypical warning or aura that many patients report is simply the manifestation of the initial simple partial seizure.
As seizure activity spreads, patients develop an impairment of consciousness and behavioral arrest during which they display stereotypical behaviors known as automatisms (e.g., lip smacking, chewing,
pulling at clothes).
In contrast to simple partial seizures, complex partial seizures are associated with postictal confusion and lethargy.
Complex partial seizures with 2° generalization:
In many patients with prolonged complex partial seizures, seizure activity can ultimately spread to involve the entire cerebral cortex. The manifestation of the “2° generalization” of the initial focal seizure activity is usually generalized tonic-clonic activity.
Generalized seizures can thus be either 1° (generalized seizure activity at onset) or 2° (initial focal activity that spreads to involve the entire cortex).
Todd’s paralysis:
Patients with focal-onset seizures often have transient (minutes to hours) focal weakness or paralysis following seizure termination. This weakness usually involves the area of the body first affected by the
seizure, providing an important clue to the focus of seizure onset.
A patient with a generalized tonic-clonic seizure who is subsequently noted to have a postictal left hemiparesis likely had a focal-onset seizure that began in the right hemisphere and secondarily generalized.
Temporal lobe epilepsy: The most common cause of simple and complex partial seizures is temporal lobe pathology, most commonly 2° to abnormalities of the hippocampus. Hippocampal sclerosis/calcification is seen on imaging. The classic auras of odd smells, sounds, or tastes are associated
with temporal lobe epilepsy.
DIAGNOSIS
If the patient has a known seizure disorder (epileptic), check anticonvulsant levels—this is usually the only test that is needed. Because therapeutic anticonvulsant levels are variable, one dose may be toxic for one patient and therapeutic for another. Therefore, take the range given in laboratory reports as a general guideline.
If the patient history is unclear or if this is the patient's first seizure:
CBC, electrolytes (K disorders doesn’t cause seizure), blood glucose, LFTs, renal function tests, serum calcium, urinalysis
CT scan of the head (urgently)—to identify a structural lesion
MRI of the brain (laters) —with and without gadolinium (first without)
An important part of the workup of a patient with a first seizure
More sensitive than a CT scan in identifying structural changes, but not always practical (e.g., in an unstable patient)
EEG: if the initial stet of diagnostic tests doesn’t reveal the etiologyof the seizure, then the EEG is performed. The EEG shouldn’t be done first
Although the EEG is the most helpful diagnostic test in the diagnosis of a seizure disorder, an abnormal EEG pattern alone is not adequate for the diagnosis of seizures.
A normal EEG in a patient with a first seizure is associated with a lower risk of recurrence.
LP and blood cultures—if patient is febrile
Laboratory values to check immediately in an unfamiliar, seizing patient
Serum calcium, Serum sodium , Serum glucose or Accu-Chek , BUN
TREATMENT
For all seizures, ABCs take priority: secure airway and roll patient onto his side to prevent aspiration.
Patients with a history of seizures (epilepsy)
Seizures in these patients are usually due to noncompliance with anticonvulsant therapy. (Even one missed dose can result in subtherapeutic levels). Give a loading dose of the anticonvulsant medication, and continue the regular regimen as before.
These patients should be chronically managed by a neurologist. Treatment with one of the standard antiepileptic drugs provides adequate control in 70% of adult patients. In another 15% to 20%, a combination regimen controls seizures.
If seizures persist, increase the dosage of the first anticonvulsant until signs of toxicity appear. Add a second drug if the seizures cannot be controlled with the drug of first choice.
If the seizures are controlled, have the patient continue the medication for at least 2 years. If the patient remains seizure-free, taper the medication(s) cautiously. Confirm this decision with a lack of seizure activity on the EEG.
Long term Rx of fisrt time seizures
Chronic antiepileptic therapy is generally not indicated after single seizure. There are several exceptions however. Treat chronically after the first time seizure in the following circumstances.
Srong family history of seizure
Abnormal EEG
Status epilepticus that required benzodiazepines to stop the seizures.
For generalized tonic-clonic seizures and partial seizures
Phenytoin and carbamazepine are the drugs of choice. They are equally effective, and side-effect profiles are similar.
Other options include phenobarbital, valproate, and primidone.
For petit mal (absence) seizures—ethosuximide and valproic acid
Medications: Focal-onset seizures are best treated with anticonvulsants such as phenytoin, carbamazepine, phenobarbital, and valproic acid. Newer medications such as gabapentin, levetiracetam, lamotrigine, and topiramate are also useful.
Vagal nerve stimulators: Although their mechanism of action remains unclear, vagal nerve stimulators can ↓ the frequency of focal-onset seizures by 25% in patients with medically refractory seizures. A pacemaker-like device is implanted in the chest with leads attached to one of the vagal
nerves
Surgery: Patients with focal-onset seizures often have an identifiable brain lesion on imaging studies. This is particularly true of temporal lobe epilepsy 2° to hippocampal lesions. In such patients with medically refractory seizures, surgical resection of the causative lesion (e.g., temporal lobectomy) can produce striking results, with up to 50–75% of patients becoming seizure free.
Patients with epilepsy who fail to respond to three trials of antiepileptic drugs are unlikely to ever become seizure free with drug therapy. Treatment-resistant patients with epilepsy should be evaluated for a surgically remediable epilepsy syndrome.
Nonepileptic seizures of psychogenic origin can be differentiated from epilepsy by their longer duration, normal electroencephalogram findings, and maintenance of consciousness.
Nonepileptic psychogenic seizures are often associated with moaning, crying, and arrhythmic shaking of the body.
COMPLICATIONS
Anticonvulsants and OCPs: Drugs that induce the liver cytochrome P-450 system (e.g., phenytoin and carbamazepine) can lead to ↓ effective levels of other medications, including OCPs. All female patients taking such anticonvulsants should be counseled to consider other means of birth control or use OCPs with high levels of estrogen.
Zonisamide, valproic acid, tiagabine, levetiracetam, lamotrigine, gabapentin, and felbamate do not interfere with oral contraceptives.
Anticonvulsants and birth defects: Use of anticonvulsants during pregnancy is associated with an ↑ risk of birth defects, particularly neural tube defects. All women of childbearing age who use anticonvulsants should be advised to take at least 0.4 mg/day of folate. Pregnant women with epilepsy
should be treated with a single anticonvulsant at the lowest therapeutic dose; valproic acid is particularly teratogenic.
Prenatal diagnostic testing should be offered. In the third trimester, vitamin K, 10 mg daily, should be administered due to depression of clotting factor levels with many antiepileptics.
Elderly patients may be particularly sensitive to the cognitive, motor, and coordination side effects of phenytoin, even if the serum phenytoin level is in the therapeutic range. Gabapentin, lamotrigine, and carbamazepine are equally effective at controlling partial onset seizures in the elderly, but gabapentin and lamotrigine are better tolerated
Valproic acid, CBZ & gabapentin are all associated with weight gain
Lamotrigine is typically weight-neutral
Felbamate and Topiramate (SE: renal stones, confusion) are associated with weight loss.
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#1
Re: SEIZURES
mtniharika - 10-05-09 14:22 STATUS EPILEPTICUS(SE)
refers to a life-threatening condition in which the brain is in a state of persistent seizure.It is defined as one continuous unremitting seizure lasting longer than 30 minutes, or recurrent seizures without regaining consciousness between seizures for greater than 30 minutes (or shorter with medical intervention). There is some evidence that 5 minutes is sufficient to damage neurons and that seizures are unlikely to self-terminate by that time.
Status epilepticus can be divided into two categories , convulsive and nonconvulsive, the latter of which is underdiagnosed
1.Convulsive
Epilepsia partialis continua is a variant involving hour, day, or even week-long jerking. It is a consequence of vascular disease, tumours, or encephalitis, and is drug-resistant.
Generalized myoclonus is commonly seen in comatose patients following CPR and is seen by some as an indication of catastrophic damage to the neocortex.
2.Nonconvulsive
Complex partial status epilepticus, or CPSE, and absence status epilepticus are rare forms of the condition which are marked by nonconvulsive seizures. In the case of CPSE, the seizure is confined to a small area of the brain, normally the temporal lobe. But the latter, absence status epilepticus, is marked by a generalised seizure affecting the whole brain, and an EEG is needed to differentiate between the two conditions. This results in episodes characterized by a long-lasting stupor, staring and unresponsiveness.
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