Dizziness & Seizures

Perspectives for Better Neurological Care
: C. Robert Adams, M.D.; Board Certified Neurologist

Dizziness, Seizures, and Spells – Oh My!

Alternative titles:

“Paroxysmal Occurrences”

“A Potpourri of Puzzling Neurologic Phenomena from Infants to Grandparents”

Accuracy in diagnosis leads to better treatment and happier patients. Using monikers to label someone “epileptic” or “a hyperventilator” can sometimes add grief to an already difficult situation. Always individualize evaluations to respect the unique character of every patient.

I. “I’m dizzy.” There are four major categories of dizziness.

A. Syncope or diminished cerebral blood flow.

1. Simple orthostatic hypotension.

2. Complicated orthostatic hypotension with iron deficiency or other factors.

3. Vasovagal phenomenon, which can occur with striking “seizure-like convulsions.”

4. Breath-holding spells, which may or may not be associated with mitigating pulmonary or cardiac disease.

5. Pulmonary causes, particularly reactive airways disease without significant or obvious wheezing (do not forget pulmonary embolism).

6. Cardiac disease of a variety of types including congenital valve disease, vascular anomalies, and even intrinsic myocardial conduction defects.

B. Vertigo or labyrinthine-like dizziness.

1. Middle or inner ear infection, inflammation, or even “just” pressure (extremely common).

2. Posttraumatic cochlear and labyrinthine dysfunction.

3. Drug-related or toxic vertigo as from antibiotics, etc.

4. Otosclerosis and ear “rocks.”

5. Structural causes, including cerebellopontine angle tumors (acoustic neuroma) and brainstem tumors.

a. (It should be noted that there is some significant overlap with these different types of dizziness.)

C. This leads us in to the third category of actual imbalance or ataxia with difficulty walking and maneuvering. (This type of dizziness is associated with a wide-based stance, stumbling, plus obvious impairment of leg and foot function.)

1. Stroke (ischemic or hemorrhagic).

2. Head trauma with or without intracranial bleeding.

3. Vascular malformations (cavernous angiomas and aneurysms).

4. Hydrocephalus.

5. Intracranial tumors.

6. Spinal cord tumors or masses causing myelopathy or spinal cord dysfunction.

7. Peripheral neuropathy as from diabetes, toxicity from drugs, vitamin deficiency, and others.

D. Last, vaguely described subjective or “cognitive” dizziness.

1. Hyperventilation with panic attacks in the setting of anxiety is always the first to come to mind; however, all the other causes of dizziness should be ruled out first. Patients with marked anxiety and panic attacks often are afflicted by other types of dizziness as well. The “hidden” problems may be generating a secondary anxiety disorder.

2. Migrainous encephalopathy.

3. Discrete psychiatric disease. Children with ADHD (attention deficit hyperactivity disorder) may feel their “mind is full” or overloaded. A racing or ruminative mind in obsessive-compulsive disorder and bipolar illness can put a child’s brain in such a “buzz” that internal feelings and behavior can be very erratic and suddenly unpredictable.

4. Interictal or postictal state with seizures, which leads us in to the next part of our talk.

II. Seizure disorders and available treatment.

A. General information.

1. A seizure disorder is a paroxysmal involuntary electrical disturbance of brain function. It may manifest as:

a. An impairment or loss of consciousness.

b. Abnormal motor activity.

c. Behavior abnormalities.

d. Sensory disturbances.

e. Autonomic dysfunction.

2. Epilepsy is defined as recurrent seizures unrelated to fever or obvious acute cerebral insult or metabolic derangement.

3. The designation “seizure disorder” is sometimes more tactful, kind, and accepted than the label of “epilepsy.” I try to reassure patients that seizure disorders or epilepsies are a very treatable entity that can be effectively dealt with just as with diabetes or asthma. A misdiagnosis of epilepsy can drastically harm and change an individual’s future.

4. Optimism that a normal lifestyle is possible should be balanced with caution of long-term or future issues. (To obtain a Nebraska driver’s license one has to be seizure free for three months before the application.)

5. Death from seizure activity or epilepsy is extremely rare. It most often occurs in individuals more handicapped by congenital brain abnormalities or acquired structural disease causing a more resistant electrical cerebral irritability in an already compromised brain.

6. More common sequelae can include risks of head and dental injuries, aspiration pneumonia, stress fractures, and especially psychosocial hindrance in school and at work.

7. Depression is common not only due to inherent predisposition, but also to effects of medications. Interictal or postictal state can be difficult to recognize and distinguish from depression. Head trauma patients with a frontal lobe syndrome can show a difficult to read appearance of flatness.

8. Etiology of seizures include:

a. Head trauma, which is a very important part of the history.

b. Stroke (ischemic or hemorrhagic infarction).

c. Metabolic derangements, particularly hypoglycemia and hyponatremia.

d. Toxic effects of drugs and chemicals, particularly psychotropics, antidepressants, stimulants, and even some antibiotics. Aspartame or Nutrasweet can in some circumstances bring out seizures and migraines.

e. Vascular malformations, particularly arteriovenous malformations, cavernous angiomas, etc., (e.g. Sturge-Weber Syndrome).

f. Infectious inflammatory processes including meningitis and encephalitis from bacterial or viral causes, etc. (A note should be made that focal infections including chronic otitis media can sometimes cause focal inflammatory injury of the brain resulting in a seizure disorder even without history of meningitis.)

g. Neoplasm or tumors of primary or metastatic character.

h. Familial hereditary epilepsy and tendencies.

i. Genetic metabolic disturbances including inherited and mutated variety (tuberous sclerosis and neurofibromatosis).

B. Diagnostic stratification of epilepsies include:

1. Etiologic:

a. Symptomatic epilepsy as due to a brain lesion; for example, traumatic contusion, stroke or tumor.

b. “Sympathetic” or accessory epilepsy due to extracerebral disturbances as from toxic drug effect, hyponatremia, or fever. With regards to the latter, benign febrile seizures tend to be “benign,” except when they are not. In particular, a febrile seizure of focal nature carries a particularly high risk for subsequent focal (partial) and partial complex seizures.

c. Essential or idiopathic epilepsy.

2. There are “lumpers” and “splitters.” As a suggestion it might be clinically helpful to be a “lumper” with regards to categorization of seizures, but a “splitter” as regards to the diagnostic of investigation, and in particular, the treatment of the disease.

3. For the classification of epileptic spells (if you are a “splitter”):

a. Simple partial or focal seizures, which begin in one discrete area on one side of the brain. There is minimal or limited impairment of consciousness.

i. Focal motor.

ii. Focal sensory.

iii. Jacksonian with spread.

iv. Versive or contraversive or “head turning” episodes.

v. Speech arrest with preserved awareness.

vi. Sensory symptoms including:

a. Visual (macropsia, micropsia, altered distance perception, etc.).

b. Auditory (a noise that is advancing, receding, louder, softer, etc.).

c. Olfactory (some symptoms can suggest localization of an irritating process or brain injury).

d. Gustatory.

e. Autonomic phenomenon (sweating, flushing, etc.).

b. Complex partial, temporal lobe, or psychomotor seizures.

i. Simple dulled attentiveness.

ii. Complex mental phenomenon including déjà vu, jamais vu, and “dreamy states.”

iii. Sudden forced emotional states such as unexplained instant combativeness.

iv. Psychosensory phenomenon such as epigastric distress or chest heaviness with emotional feelings that can range from mild anxiety to intense terror.

c. Partial seizures secondarily generalized. (Phenomena can include jacksonian spread and Todd’s or postictal paralysis.)

d. Generalized seizures occur with bilateral brain electrical irritability and instability without obvious focal onset.

i. Simple absence seizures only with impairment only of consciousness.

ii. Complex absence seizures include other phenomenon on top of the alteration of consciousness, such as:

a. Myoclonic jerks or myoclonus.

b. Increased in postural tone.

c. Atonic types with loss of postoral tone.

d. Automatisms as with lip smacking and blinking.

e. Autonomic phenomenon including episodes associated with enuresis. (All bedwetting is not due to delayed physical and social maturity.)

iii. Myoclonic epilepsy. (Not all myoclonic jerks are epileptic, benign nocturnal myoclonic jerks are, of course, common. Myoclonic jerks can occur in addition due to spinal cord disease and other structural injuries to the CNS.)

iv. Infantile spasms.

a. The West syndrome is a triad of infantile spasms, mental deterioration, and a characteristic EEG picture of hypsarrhythmia. This syndrome usually develops between 3 and 12 months of age, and the spasms have usually stopped before age 5, often transitions to other types of seizures. The presentation is significant in that infantile spasms or “salaam attacks” can be mistaken for colic. The spasms often occur in clusters in the early morning or upon awakening from a nap with the baby doubling up as if in pain and often crying afterwards.

v. Clonic seizures.

vi. Tonic seizures.

vii. Grand mal or tonic-clonic seizures.

vii. Atonic seizures, particularly episodes that cause “drop attacks.”

ix. Akinetic seizures or loss of movement, although without loss of muscle tone.

e. On the other hand, if one was a “lumper,” one could grossly consider two major types of seizure disorders:

i. Generalized seizures tend to cause unresponsiveness and bilateral or non-focal motor phenomenon. There is no obvious structural cause.

ii. Focal or partial complex seizures originating on one side of the brain and often suggesting discrete structural or identifiable etiologic injury to that side of the brain.

C. It is often difficult to assess impairment of consciousness in neonates, infants, and very young children. Neonatology is, of course, a very delicate super specialization. The clinical presentation of seizures in infants can be very subtle, nonspecific, and non-stereotyped.

D. Diagnostic workup of a seizure should include:

1. Historical clarification of familial predisposition as well as prior injuries or cerebral insults, and in particular, head trauma. (Again, tuberous sclerosis and neurofibromatosis are common.)

2. Metabolic workup including at least chem profile with blood sugar and sodium level, magnesium, T4, TSH, serum iron studies, plus serum ferritin, adding more complex metabolic screens and genetic analysis depending upon the suggestive circumstances. A lead level may be indicated. A drug screen can be important, particularly to catch elicit drugs as with stimulant abuse.

3. An EEG or electroencephalogram, which helps in clarifying:

a. Presence or absence of electrical irritability (a “normal” EEG does not absolutely rule out a seizure disorder). Recurrent, unexplained stereotype events may merit an empiric trial on anticonvulsants. A positive response to treatment, however, does not necessarily confirm a diagnosis of epilepsy. In particular, migraine phenomenon, panic attacks, and labile psychiatric changes can also respond positively to some of the newer “broad spectrum” anticonvulsants. Some of the newer agents, for instance lamotrigine, can be very useful psychiatrically as a mood stabilizer.

b. Assessing frequency of electrical discharge and to help in assessment of the threshold for further seizures.

c. May help to judge the therapeutic benefit to a medication; however, do not chase the brain wave test just to try to normalize it. The seizure patient should be treated clinically, hoping to improve but not necessarily normalize the EEG.

d. Lateralization to one side of the EEG to suggest focal structural disease.

e. More definitive diagnosis in some cases from the EEG alone

f. Brain mapping.

4. Ancillary tests to clarify manifestations of systemic disease:

a. Chest x-ray to see pneumonia.

b. An echocardiogram to identify congenital vascular abnormalities and valvular disease in the heart, which could be a source of emboli.

c. A spinal tap if meningitis is suspected.

5. Brain imaging.

a. CT scanning with contrast is the “gold standard” for identifying hemorrhage and clarifying traumatic injuries and as a tool to screen for aneurysms and vascular malformations.

b. Magnetic resonance imaging (MRI) is more sensitive for posterior fossa or brainstem and cerebellar disease and for “subtle lesions” in the temporal areas.

c. Magnetic resonance angiography (MRA) has in many cases replaced the more tedious and injurious catheterization that was formerly needed for identification of aneurysms and vascular malformations.

d. Positron emission tomography (PET) is used in evaluating focal metabolic function in different areas of the brain.

E. Palliation or treatment of seizure disorders. I think it would be most useful to go backwards or reverse in describing the most drastic or “heroic” treatments then moving to easier and common sense suggestions:

1. Brain resection of not only obvious neoplastic processes but also of resistant irritable electrical scar foci.

2. Ketogenic diet (besides being distasteful, long-term vascular disease is a concern).

3. Vagus nerve stimulation.

4. Drug therapy (to be further discussed).

5. Correction of modifiable derangements including infection as from septicemia or meningitis; metabolic disturbances, particularly hyponatremia, hypomagnesia, and hypocalcemia; and removal of toxic provocation as with aminophylline. (There is almost no reason to use aminophylline any more with the asthma treatments now available.)

6. Never forget to counsel with regards:

a. Avoiding fasting or skipping meals.

b. Getting regular sleeping hours, particularly not enough sleep but also considering issues of disturbed circadian rhythms and excessive sleeping.

c. Avoidance of alcohol, particularly alcoholic binges.

d. Caution with regards to flickering stimuli as from video games.

e. Do not overestimate or “push” the issue of stress as a reason for the medical problem. Never forget that all medical problems cause significant stress and anxiety even as apart from pre-existing psychiatric tendencies and conditions.

F. Drug treatment.

1. Common or “class action” side effects are:

a. Dizziness, including ataxia and vertigo.

b. Somnolence.

c. Asthenia (fatigue).

d. Mental slowing, including problems with word finding. (This is an important issue in children who are developing their thought patterns and speed of communication.)

e. Personality change. (Depression, new onset aggressive tendencies, and even simple loss of enthusiasm.)

f. Headaches.

g. Gastrointestinal tract upset.

h. Rash.

i. Usually occurs within several days to up to six to eight weeks but not always.

ii. Make sure the drug is the culprit. Do not be fooled by:

a. Poison ivy.

b. Bug bites.

c. Allergies to other substances including foods, skin care products such as lotions and soaps.

d. Viral and other infections.

e. Other drugs.

f. Photosensitivity, although without “true” rash.

iii. Prominent rash on the trunk probably promotes more suspicion for skin reaction to the anticonvulsant.

iv. Clarification of an anticonvulsant rash or sensitivity is critical to not “burn bridges” with a therapeutic approach that may be desperately needed in the future.

v. If an antiepileptic drug (AED) is a suspected cause of a rash, always stop the drug due to possible relentless progression to Stevens-Johnson syndrome or toxic epidermal necrolysis.

i. Interference with the effects of oral contraceptive drugs.

j. Disturbances of weight regulation (changes in appetite).

k. Exacerbation or alteration of seizures can occur. Take the family seriously if they report increased seizures or other new phenomena are associated with the institution of the drug.

l. Unique side effects.

i. Blood dyscrasias including aplastic anemia as from felbamate (Felbatol).

ii. Hepatic failure as from felbamate (Felbatol) and valproic acid (Depakote ER). It should be clarified that phenytoin (Dilantin) very commonly causes a “reactive” elevation of liver enzymes that can be followed and is not necessarily harmful or consequential. Valproic acid can cause troublesome hyperammonemia even without obvious liver enzyme disturbance.

iii. Gingival hyperplasia as from phenytoin (Dilantin).

iv. Nephrolithiasis from topiramate (Topamax) and zonisamide (Zonegran).

v. Open-angle glaucoma as from topiramate (Topamax).

vi. Hyponatremia from carbamazepine (Tegretol, Carbatrol) and to a lesser extent oxcarbazepine (Trileptal).

vii. Teratogenic effects, particularly neural tube defects in the setting of valproic acid or Depakote. This adverse effect has serious future implications in a young girl who may at some point in the future become a perspective mother.

2. Concerns in pregnancy:

a. Always maintain folic acid supplementation.

b. Consider diagnostic testing at 14-20 weeks with alpha-fetoprotein levels and structural ultrasound.

c. With regards to birth defects in animals and in early clinical studies, the newer anticonvulsants seemed to have a favorable profile and most are Class C.

3. Specific drugs:

a. Phenobarbital has horrendous side effects (avoid if possible).

b. Phenytoin (Dilantin, Phenytek, and IV Cerebyx)

i. Very effective except in certain seizure types excluding absence or myoclonic epilepsy.

ii. It has the advantage of a “therapeutic window,” when tends to be very protective in the range of 10-20 but with ataxia and lethargy over that level.

iii. It can often be given in a once-daily dosage as compared to most of the other anticonvulsants needing a scheduled multidose regimen.

iv. Always advise parents to vigorously shake Dilantin and other suspensions due to variable bioavailability.

c. Valproic acid (Depakote).

i. Although very useful, it has not quite lived up to its original “billing” as the “all purpose anticonvulsant.”

ii. The extended-release formulation sometimes lessens side effects of limiting nausea.

iii. Weight gain is often a big issue.

iv. It is very effective for a variety of seizure types, particularly absence, myoclonic, generalized tonic-clonic convulsions, and helpful but somewhat less useful for strict partial or focal seizures.

v. Never forget the issue of teratogenicity in females (young girls may some day become mothers).

d. Carbamazepine (Tegretol, Carbatrol).

i. Often the “gold standard” used for controlled comparison in studies of benefit of anticonvulsants.

ii. Diplopia, lethargy, and disturbed gait can be quite striking when carbamazepine is initiated. Slow titrations are important.

iii. Possible favorable behavioral effects such as decreased anxiety, improved mood, and decreased aggression.

iv. Used as a mood stabilizer for bipolar illness.

v. This has been the standard pregnancy drug, although the newer agents are all primarily Class C.

e. Lamotrigine (Lamictal).

i. Approved FDA indications include:

a. Bipolar disorders in patient greater than age 18.

b. Adjunctive treatment for partial seizures in pediatric patients greater than and equal to 2 years of age.

c. There is optimism for significant help in other conditions including new-onset typical and atypical absence seizures, generalized tonic-clonic seizures, atonic and myoclonic seizures, and the difficult to treat Lennox-Gastaut syndrome.

ii. Rash can occur as it does with other drugs, particularly carbamazepine.

iii. Due to “antigen-loading phenomenon” titration should be slow especially when added to valproic acid. Depakote greatly increases the half life of lamotrigine.

iv. The combination of lamotrigine and valproic acid has been very effective in very difficult, resistant epilepsies, even those who have sometimes failed ablative brain-resection surgery.

f. Gabapentin (Neurontin).

i. It has a 95-100% renal excretion and no appreciable interactions with other drugs.

ii. Efficacy in partial complex and mixed-seizures disorders is comparable to carbamazepine.

iii. It has an idiosyncrasy of a slower absorption with greater increasing doses due to saturation kinetics.

iv. Success as an antineuralgic agent in palliating intractable pain and in treating migraines.

v. Elderly patients can be susceptible to its sedative and depressant effects.

g. Oxcarbazepine (Trileptal).

i. This is approved as being very effective for partial and mixed seizures in ages 4 and over. Studies suggest tolerance and possible safety even used in children down to less than one year of age.

ii. As with carbamazepine, Trileptal has been helpful in treating chronic and intractable pain.

iii. Less hyponatremia tends to occur than with carbamazepine.

iv. Tolerance and efficacy with careful titration also tends to show a positive trend as compared to carbamazepine.

h. Levetiracetam (Keppra).

i. As with Neurontin, a primary renal excretion limits interactions with other drugs.

ii. Possibly less sleepiness or fatigue.

iii. Minimal systemic adverse effects.

iv. Occasional worsening of mood and behavior.

v. It tends to cause less cognitive impairment than some other anticonvulsants.

vi. Starting dose can be a therapeutic dose (500 mg p.o. b.i.d. in an average adult).

i. Topiramate (Topamax).

i. Besides help in control of partial seizures and generalized tonic-clonic events, benefit in the Lennox-Gastaut syndrome and with infantile spasms has been shown.

ii. This drug has been extremely helpful in prophylaxis of very intractable migraine events.

iii. Metabolic acidosis with altered sodium bicarbonate levels can occur, although usually without clinical symptoms.

iv. Cognitive side effects can include problems with “word finding,” which would be distressing with a developing young mind.

v. Tolerance tends to be “black or white.” If it induces dysphoria, it has to be discontinued.

j. Zonisamide (Zonegran).

i. It is a sulfonamide with consideration of allergic sensitivity to sulfa.

ii. Possible once-a-day dosage.

k. Tiagabine (Gabitril).

i. Useful for partial seizures as well as treatment of migraine and neuropathic pain, especially with spasticity.

ii. Can be useful as a nighttime hypnotic for insomnia.

l. Ethosuximide (Zarontin).

i. It has been helpful in the control of absence seizures.

m. Clonazepam (Klonopin).

i. An adjunct in the management of “breakthrough” seizures, particularly in the setting of marked anxiety, nervousness, and sporadic myoclonic jerks.

n. Rectal diazepam (Diastat) has been useful in some circumstances to stop a cycle of “breakthrough” seizures, preventing a visit to the emergency room.

o. Anticonvulsants in summary:

i. Narrow spectrum AED’s.

a. Most useful in focal, partial complex, and seizures secondarily generalizing from a focal source.

1. Phenytoin (Dilantin).

2. Carbamazepine (Tegretol).

3. Oxcarbazepine (Trileptal).

4. Gabapentin (Neurontin).

ii. Broad spectrum AED’s.

a. Effective for generalized seizure types such as absence, tonic, tonic clonic, myoclonic, and atonic.

1. Ethosuximide (Zarontin, for simple absence seizures only).

2. Valproic acid (Depakote).

3. Lamotrigine (Lamictal).

4. Topiramate (Topamax).

5. Zonisamide (Zonegran).

iii. Monitoring drug levels.

a. As opposed to the monitoring required with phenytoin, valproic acid, and carbamazepine, the “newer” anticonvulsant agents are more empirically administered and titrated often without need for tedious and obsessive drug-level testing.

iv. Low risk of cognitive side effects:

a. Lamotrigine (Lamictal).

b. Levetiracetam (Keppra).

c. Felbamate (Felbatol).

d. Oxcarbazepine (Trileptal).

v. Minimal drug interactions:

a. Gabapentin (Neurontin).

b. Levetiracetam (Keppra).

vi. Helps promote weight loss.

a. Topiramate (Topamax).

b. Zonisamide (Zonegran).

c. Felbamate (Felbatol).

d. Lamotrigine (Lamictal) tends to be neutral with regards to weight gain.

vii. With regards to efficacy in partial and mixed seizure disorders:

a. Phenytoin is comparable to carbamazepine. The latter has been the standard with which to compare the new anticonvulsants.

b. Lamotrigine is comparable to phenytoin and carbamazepine.

c. Oxcarbazepine is effective as carbamazepine but possibly less rash, hyponatremia, and adverse CNS side effects, particularly with careful titration.

III. Enlightening cases.

A. A 10-year-old “princess” turned “devilish.”

Resolution: A truly angelic straight-A student was turned into an obnoxious biting monster by “innocent” use of Dimetapp by her parents. A switch to Allegra-D allowed her to revert back to her normal personality.

B. A 5-month-old girl with spells of “shuddering.”

Resolution: Multiple EEG studies in an infant with clusters of shuddering spells over a several-week period failed to reveal any answer. Eventual treatment of urinary tract abnormalities leading to recurrent infection stopped the vasovagal phenomenon that was associated with that irritation.

C. A 10-year-old handicapped girl with a history of multiple shunt revisions for hydrocephalus having spells of intermittent jerking with lethargy not responding to triple anticonvulsant therapy.

Resolution: Her antiepileptic drugs were associated with marked sedation and personality change but did not help in decreasing spells of sudden altered consciousness with variable intermittent drop attacks. After nine months of repeated CT scans and pleadings with the neurosurgeon, another shunt revision was done showing not only blockage but also shunt infection. The spells and drop attacks were eliminated with much improvement in her personality. This allowed the tapering and elimination of her anticonvulsants that were causing serious sedative side effects.

D. A 14-year-old female basketball player with paroxysmal exertional dizziness stopping her play.

Resolution: Seizure disorder, cardiac disease, and common teenage girl problems of orthostatic hypotension and iron deficiency were ruled out. Treatment of “silent” asthma (marked exertional-related reactive airways disease without wheezing) was made with Singulair and beta-adrenergic inhalers. She was then able to achieve her high-athletic potential without spells.

E. A 7-year-old with recurrent salivation and drooling in the setting of persistent and chronic rhinitis and postnasal drip.

Resolution: Antihistamines and decongestants in multiple trials failed to provide any benefit. Benign childhood epilepsy or Rolandic epilepsy was present with the presentation of postnasal drip and drooling. After EEG identification, there was complete elimination of episodes with low-dose carbamazepine.

F. A 9-year-old baseball player with sleep onset jerks and twitches.

Resolution: Nocturnal disturbances of jerks and twitches turned out to be focal seizures caused by the glancing blow of a baseball as it slipped out of the young outfielder’s hand, hitting his head one year prior. Gabapentin (Neurontin) halted the nighttime problems without slowing the cognitive function in this straight-A student.

G. A 9-year-old boy being considered for diagnosis of Tourette’s syndrome due to tics, twitching, and multiple “restless” behaviors.

Resolution: Caution should be made in jumping to treatment with antipsychotic tranquilizers for tics. The following discoveries were made:

1. Squinting with facial twitching and grimacing was eliminated by prescription glasses for impaired vision.

2. Antihistamine treatment stopped the recurrent throat clearing that was a subject to ridicule for this boy in class.

3. His odd barking cough resolved with treatment of his reactive airways disease with bronchodilators.

4. His restlessness with limited ability to sit still was essentially eliminated by treatment of his chronic constipation with his infrequent “once a week bowel movements.” The end result of this was elimination of his distracting behavior with no need for tranquilizers over a three-year followup.

5. All tics are not Tourette’s.

Rev.040105

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