___ he diagnosis of paroxysmal events in I the elderly presents particular difficulties, especially when contrasted with the problem presented by younger patients. In the first instance, the history is often difficult to obtain, vague, or not available at all. A second problem, common in the elderly, is the coexistence of multiple medical and/or neurological problems that complicate the analysis of intercurrent paroxysmal symptoms. A third factor involves the confounding results of diagnostic studies, for example, electroen-cephalographic (EEG) findings or the results of studies of the cerebrovascular system that either may help to elucidate an obscure event or series of events, or serve to obfuscate diagnosis.
Perhaps the best way to approach the diagnostic dilemma is to understand the general characteristics of epileptic seizures in the elderly population, and then draw a contrast with the presenting symptoms in a particular case. The most common type of epileptic seizure in the aged is the complex partial (CPS)—up to 40% of those presenting with new onset seizures (1). In some cases, the CPS is typical in its characteristics. That is, it begins with a motionless stare, followed by a period of automatisms. There is postictal confusion and perhaps reactive automatisms during the postictal state. These events are relatively easy to recognize and are usually not confused with other conditions. By contrast, the CPS often does not conform to this progression of symptoms. A period of unresponsiveness or clouded consciousness, without obvious motor activity, is common. Such events are usually short-lived, lasting perhaps minutes. A postseizure confusional state follows but may not be profound. The patient may be, and usually is, unaware of having such seizures and, indeed, may be hard to convince when the diagnosis is suggested. Table 8.1 list those imitators of epilepsy frequently occurring in the elderly population.
A common problem in the aged is an episode of unconsciousness for which there are no historical details. Typical is the person found on the floor, say beside the bed or in the bathroom. Upon discovery, there is no motor activity or other features suggestive of an epileptic attack. Usually the duration of unconsciousness is unknown, although it may be suspected, based on such factors as when the person was last seen, when there was no answer to the telephone, or when the person was known to arise in the morning. The person may be recovering when found, may or may not be confused,
Imitator of Epilepsy
Light-headed warning, brief LOC without achieving horizontal position, a few brief convulsive movements,little or no postictal confusion
Simple forgetfulness; continual memory loss without obvious fluctuation
Nonspecific term, may be "lightheadedness" or even vertigo; no alteration of awareness
Transient hemiparesis or hemisensory loss;
may be manifested by aphasia; minutes to hours
Memory registration intact; failure of second stage memory, able to respond and carry out complex acts;repeated questioning; duration: hours; sometimes confused with CPS
Altered mental status: confusion, lethargy; coma; may fluctuate; myoclonic jerks (multifocal); epileptic seizures may occur; abnormal laboratory studies; may be typical EEG findings such as triphasic waves
If there is a warning, likely to be RES; LOC 1-2 min. with generalized convulsive movements, tongue bite (sometimes), postictal confusion that may be prolonged.
Fluctuating memory loss; restricted duration; stereotyped; may not be aware of the occurrences
Vertigo may be a manifestation of a seizure, followed by clouded consciousness or confusion; stereotyped events
Hemiparesis/hemisensory loss rare as epileptic manifest; aphasic seizures are described; differentiation from TIA may be difficult; EEG or video-EEG monitoring studies are required (in addition to vascular studies)
CPS duration 1-2 minutes on average; automatisms; altered awareness; often a warning (e.g., RES); postictal confusional state that may be prolonged; EEG likely to be to be abnormal with epileptiform discharges
Nonconvulsive status epilepticus may have similar clinical manifestations; fluctuations in mental status may be more evident; seen in multisystem disease, benzodiazepine or psychotropic drug withdrawal, as a sequel to generalized epileptic seizures. EEG: generalized epileptiform activity; responds to antiepileptic drugs such as benzodiazepines (and others)
RES: rising epigastric sensation; LOC loss of consciousness; CPS: complex partial seizure and usually has no memory of the event. Any possible premonitory symptoms may not be remembered.
In these cases, the examination may offer substantial clues. For example, is there evidence of bruising or other injury? Is there evidence of breakdown of the skin? Are there signs of fracture? Is there an apparent head injury? Could the patient have had a syncopal attack and struck his head, thus accounting for the unresponsiveness? Was she hypoglycemic? On neurological examination, there may be no focal or lateraliz-ing findings. Conversely, there may be neurologic signs pointing to a focal brain lesion, such as a new CVA. These are only a few of the possible factors that might suggest an etiology. Clearly, a complete medical and neurological evaluation is indicated. The problem is that investigations may be unrevealing, equivocal or, as is commonly the case, reveal several concurrent abnormalities, say cardiovascular, metabolic, and neurologic.
An obvious consideration is an epileptic seizure, even though there may be no history of seizures. New onset seizures are quite common in the elderly, the majority being secondary to cerebrovascular disease including acute stroke, silent stroke, and diffuse small vessel disease (2,3). In cases without history or observation, a definitive diagnosis may be impossible. Many will rely on the EEG, which should be performed in all such cases. Discovery of a spike focus or other paroxysmal phenomena may tilt the balance toward seizure occurrence. When such are absent, however, a diligent search for another etiology is mandatory. Unfortunately, when all studies are unrevealing, the clinician may be forced to observe the patient, or treat empiri cally with an antiepileptic drug—not an ideal choice but one often selected.
We frequently encounter this nonspecific complaint, and it is always difficult to unravel. The patient usually means episodes of unawareness or lack of any memory for a time. The differential diagnosis obviously must include seizures, most particularly CPS, for which the patient has no memory. The EEG may aid in making the diagnosis if there is no available history from a family member or other reliable observer. If the EEG is unre-vealing, the diagnostic problem remains. Other considerations include transient global amnesia (TGA) and transient ischemic attacks (TIAs) involving the posterior circulation. One should bear in mind the possibility of alcohol or drug use. Alcoholism is more common in the elderly than usually recognized, and drug use is not rare (4,5). The elderly brain is ill-equipped to cope with the effects of substance abuse, and episodic loss of memory would be expected. Although the patient may be reluctant to reveal his use of these substances, the physician should be aware of this possibility and specifically take an alcohol and drug history.
Drop attacks have always presented difficulties in diagnosis, and there still is no unanimity concerning their cause (6). Such attacks are truly frightening in that the patient, usually in later years, suddenly drops to the floor without warning. The person usually is able to arise very soon after the fall and commonly denies loss of consciousness. There may or may not be a brief postevent confusional state. A common school of thought ascribes the attacks to basilar-vertebral insufficiency; that is, an acute decline in blood flow to the posterior circulation. In this formulation, the ischemia disables the reticular activating system as well as the motor system. Thus, the patient falls suddenly. Evaluation includes studies of the posterior circulation, including transcranial Dopplers, and of the cardiovascular system. Whereas arteriosclerotic disease of the vessels may be found, it may seem insufficient to explain the symptoms. Such patients may suffer from intermittent arrhythmias or even Stokes-Adams attacks, resulting in acute ischemia. In these instances, EEG studies would not contain epileptiform discharges. With these factors in mind, one may consider whether drop attacks can be epileptic in origin. The answer is yes, although an epileptic seizure characterized solely by a sudden fall with no postictal phase would be unusual. The entity known as temporal lobe syncope is characterized by sudden falls without significant motor activity. There is a following confusional state, suggesting an epileptic origin. The diagnosis becomes more evident if a past history of typical CPS is obtained. The EEG is likely to show a temporal lobe abnormality, supporting the diagnosis. If the EEG is unrevealing, or if the typical history is not available, the events are more likely to be ischemic in origin.
There is a tendency for non-neurologists to diagnose syncope in elderly patients who have episodes of unconsciousness. Syncope is a condition with a constellation of symptoms that differentiate it from epilepsy. Well known is the premonitory symptom of "light headedness," variously described as blood draining from the head or wooziness. The patient rapidly loses consciousness and falls to the ground. The duration of unawareness is brief, with adequate cerebral circulation being established rapidly in the horizontal position. Postsyncopal confusion is brief or absent. These features discriminate syncope from epilepsy. Note, however, that syncope is sometimes accompanied by brief clonic movements or tonic postur-ing—convulsive syncope (7). Convulsive syncope is more likely to appear if, when the patient faints, the patient remains relatively upright, for example when a faint occurs in an easy chair, or when someone nearby attempts to prevent the patient from falling. Despite the motor activity, convulsive syncope retains the other features of the uncomplicated condition. Note that patients with syncope do not have epileptiform EEG findings. The evaluation must include a detailed cardiovascular work up as well as an evaluation of the patient's medications (8,9) (see also Chapter 17).
Memory disturbances, especially when intermittent, present a truly vexing problem. As any neurologist or epileptologist knows, memory difficulties are one of the most frequent complaints in the consulting room. Of course, the nature of the memory complaint is key to a working diagnosis. Simply forgetting where one last placed a set of keys, or forgetting to add a loaf of bread to a shopping list, does not raise much suspicion of an ictal event. On the other hand, not recalling how one got to the parking lot from the store, perhaps a period of several minutes, or passing one's subway stop without recall, certainly would raise the question of an ictal event. Such lapses may occur without any evidence of organic disease, and only detailed neurological investigation will provide the answer.
A related episodic disturbance is the occurrence of staring spells. Yes, people stare frequently. If one observes such staring, particularly when devoid of motor activity, it is impossible to know what is happening in the brain of such a person. Daydreaming? In thought? Tuned out? It is important to understand that epileptic seizures in the elderly not infrequently are characterized by motionless staring. The patient usually is completely unaware of being "absent," and if confronted will vigorously deny it. The key to diagnosis is stereotypy—that is, the recurrent events are similar in duration. A good observer might see some minor automatisms, less evident than in typical CPS. Again, the EEG may provide diagnostic support for CPS, and if it does, any abnormality will be focal or lateralized. If the EEG is unrevealing or nonspecific, the clinician may institute treatment on the basis of the clinical picture. Bear in mind that few neurologic conditions produce stereotyped symptoms of this type, and a diagnosis of epileptic seizures is likely.
The elderly patient with dementia presents particular and often confounding problems when it comes to episodic symptoms resembling seizures. As anyone knows who has experience with patients in nursing home care units, those with dementia exhibit many intermittent behaviors such as staring, apparent orofacial and other automatisms, temper outbursts, wandering, fluctuating confusion, and memory lapses, to name a few. All these phenomena could well be ictal events, and all could simply be related to the dementing process. Unfortunately, many nursing home facilities have a relatively limited number of visits by physicians, who generally spend limited time with individual patients and who may have limited neurologic experience. It is probable that epileptic seizures would not be a consideration to explain the episodic behaviors mentioned above. In a study of patients in three nursing homes who were receiving antiepileptic drugs, it was found that EEGs were seldom ordered (10). In fact, few EEG reports were available in the records. The answer to this diagnostic dilemma lies in an educational process to raise awareness of the possibility that some patients may suffer from seizures in a setting of dementia. More liberal use of neurologic consultations and EEG studies could result in appropriate treatment and improved quality of life for many.
This is one of the most common complaints the neurologist encounters. The problem is that there is no uniform definition of the term. In fact, each patient has his or her own experiences that lead to a complaint of dizzi ness. The most obvious and understandable type of dizziness is true vertigo, meaning a sudden feeling of rotation or displacement in space. True vertigo can be a manifestation of CPS, but in this setting it rarely is an isolated symptom. Nonetheless, the evaluation of a patient with true vertigo should include an EEG. More difficult to interpret are other forms of dizziness such as light-headedness, or a vague feeling in the head that the patient cannot describe. Such complaints are difficult to evaluate. Close inquiry may reveal that the patient is not "clear" with his or her thoughts, or feels a little confused. Again, the problem is determining whether the complaints are episodic or continual. In episodic cases, epileptic seizure activity is a distinct possibility. Again, one of the major problems in assessment is establishing whether there is an episodic or stereotyped pattern of symptoms. In a setting of dementia, this may be difficult. In any event, evaluation including EEG studies is indicated.
Transient ischemic attacks (TIAs) are sometimes confused with epilepsy, although the two conditions are quite distinct with respect to their clinical features. The transient occurrence of hemiparesis or hemisensory loss (numbness, deadness) is well known. Such negative symptoms, although not unknown, are rare manifestations of epileptic seizures. Somewhat more problematic is the transient occurrence of dysphasia or aphasia. While more likely to be a TIA than a seizure, aphasic seizures are well known (11). Generally speaking, ictal aphasia is progressive, developing over time from dys-nomia or hesitancy of speech, through paraphasic errors, and culminating in a global aphasia. This process may take several minutes or even more. When the EEG discharges subside, progressive improvement occurs. Aphasia resulting from a TIA, whether complete or incomplete, tends to occur suddenly and, after a time, resolves more quickly. These features are admittedly generalizations but they can provide clues as to the true nature of the disturbance. The evaluation of episodic aphasia must include cerebrovascular studies and an EEG. If event frequency permits, video-EEG monitoring should be carried out in an attempt to record the clinical and electrographic features of the language disturbance.
Transient global amnesia (TGA) is a condition characterized by the abrupt onset of memory loss, usually in older persons. The patient is awake and able to carry out many normal activities. Memory registration appears to be intact, thus allowing the patient to converse or carry out relatively complex acts. Such patients typically are confused to some degree and typically ask questions repeatedly such as "where are we now, where are we going?" and the like. In the past, an attack of TGA was thought to be a once-in-a-lifetime event lasting 24 hours (12). Subsequent experience has shown that multiple events may occur, and that the average duration is considerably shorter, on the order of 9 to 11 hours (13).
Over the years, the cause of TGA has been the subject of controversy. Originally thought to be epileptic in nature, this turned out not to be the case. The EEG is normal, or at least contains no epileptiform activity. In fact, an EEG recording during an attack of TGA demonstrated a normal background with no paroxysmal discharges. It is likely that most attacks of TGA are due to ischemia involving both temporal lobes. TGA has also been described in younger patients without evidence of cerebrovascular disease. In these cases a mechanism similar to migraine has been proposed (14).
The differential diagnosis of TGA includes CPS. Whereas the duration of TGA would appear to be inconsistent with CPS, the elderly often have prolonged postictal states following a brief seizure. If the seizure itself is unobserved, the postseizure confusional state with memory loss may mimic TGA. A thorough evaluation including EEG studies should settle the issue. Although not usually possible, an EEG performed while the patient is symptomatic would provide support for the true diagnosis (see also Chapter 17).
One might think that patients with tremor or clonus would not qualify as those with paroxysmal disturbances resembling epilepsy. From time to time, however, we receive an EEG request with a brief history such as "patient with intermittent tremors, rule out seizures." Such patients usually have parkinsonism with intermittent rhythmic tremor at about 4 to 6 Hz. The EEG is devoid of epileptiform activity, but tremor artifact may be prominent, either unilateral or in the occipital regions due to transmission of the tremor to the head. Although the artifact may superficially resemble epilep-tiform activity, the lack of a potential field and correlation with recording from an EMG electrode will confirm the diagnosis.
In cases of referral for rhythmic motor activity due to clonus, a neurologist (who would immediately recognize the condition) usually has not seen the patient. Our technologists make the diagnosis by observation, and the EEG is nonepileptiform.
Myoclonic jerks present difficulty in diagnosis, especially when associated with an altered mental status. In many cases, the cause is fairly clear: for example, patients with renal failure who develop multifocal myoclonic jerks. This motor activity is not epileptic in nature and reflects the metabolic encephalopathy. The clinical picture may be complicated if the patient develops a seizure. In these cases, the myoclonus may well be regarded as part of an epileptic diathesis. Seizures are not particularly unusual in metabolic encephalopathies. Moreover, the EEG may reveal some multifocal sharp waves, thus further compounding the diagnostic dilemma. These patients do not have epilepsy, and the seizure and/or the myoclonic jerks are secondary to the metabolic derangement. Nonetheless, they often are treated with antiepileptic drugs. If so, the treatment should not be continued after the patient has stabilized.
Although it may appear that a metabolic encephalopa-thy in the aged would present no diagnostic difficulties, the opposite is the case. Hepatic, renal, and electrolyte disturbances are common, as are sepsis and drug intoxications. In all these cases, the patient may present with altered mental status including confusion, disorientation, lethargy, and even coma. The changes in mental status may be continuous or discontinuous; in fact, intermittent confusion is common. For example, in cases of hepatic or renal encephalopathies, such patients are usually well known to suffer from renal or hepatic disease. Thus, when they present with increasing confusion, the assumption is that the known medical condition is the cause. Routine laboratory studies may reveal an increase in BUN/creatinine or deranged liver function tests. Conversely, there may be little change in the numbers from previous known levels. In the latter case, one may question whether another cause for mental status fluctuations exists. Here the EEG may offer important diagnostic information. Typical EEG findings are present in metabolic encephalopathy, such as background disorganization, diffuse slowing and, importantly, triphasic waves (15,16). Although triphasic waves are typical in hepatic encephalopathy, they are also found in renal and other metabolic disturbances. However, the EEG may reveal continuous or discontinuous epileptiform activity, suggesting strongly that CPS is responsible for the patient's presenting symptoms.
With respect to other systemic diseases—sepsis is a good example—the patient often presents with lethargy and confusion due to the toxic effects of the infection.
In most cases, the EEG reveals poor organization and diffuse slowing along with bifrontal delta activity. However, in others, epileptiform discharges may be recorded, suggesting the possibility of clinical epileptic seizures. The risk of epileptic seizures is likely to be increased if the patient has a pre-existing cerebral lesion, such as an infarct. Although the patient may develop obvious clinical seizures characterized by generalized or focal motor activity, the confusional or lethargic state may be a manifestation of CPS.
Mention should be made of conditions such as hypoglycemia and hypocalcemia. The patient may present with generalized tonic-clonic convulsions and even status epilepticus. In some cases, focal or even multifo-cal seizures may occur. Rapid correction of the metabolic defect is essential, as is the prompt administration of an intravenous antiepileptic drug. These patients, of course, do not have epilepsy, and chronic antiepileptic drug administration is not required.
Prescription drugs, such as psychotropic agents may lead to a toxic encephalopathy. The aging brain is particularly prone to medication side effects (17,18). Intoxications may be manifested by such central nervous system (CNS) symptoms as unsteadiness or dizziness. In addition, confusion and lethargy may result. Again, the EEG will be helpful in differentiating possible seizures from encephalopathic fluctuations in mental status (see also Chapters 14 and 15).
Nonconvulsive status epilepticus (NCSE) is indeed an epileptic condition and not an imitator of epilepsy. Thus, the reader might well be curious regarding the inclusion of this entity in this chapter. In fact, the reverse is true. NCSE is an imitator of nonepileptic conditions such as metabolic encephalopathies and, as such, is underdiagnosed and inappropriately treated (19). Therefore, it seems rational to include a discussion of NCSE here in order to complete the circle of "diagnostic deception" in the elderly.
There are two broad subdivisions in NCSE: absence and complex partial. Absence NCSE occurs mainly in children and is not considered in this discussion. Complex partial NCSE occurs in many settings and is not infrequent in the aged. Further, the clinical manifestations are diverse, ranging from modest confusion or personality change to apparent sleep or coma.
Situations particularly likely to reveal complex partial NCSE include:
• Failure to recover full awareness after general anesthesia
• Cerebral hypoxia
• Multisystem disease
• Drug withdrawal (e.g., benzodiazepines and psychotropics)
• Failure to recover after a generalized tonic-clonic convulsion
In all the above conditions, the underlying condition is assumed to be the cause, and often this is true. Take the example of delayed recovery after a prolonged operation under general anesthesia. There may have been a hypotensive episode, or a particularly difficult procedure with considerable bleeding. Under these circumstances, one might not expect immediate recovery. With the passage of time and continued unresponsive-ness, a neurologist may be summoned for an opinion. Examination reveals alteration of consciousness, perhaps coma. There may be little or no minor motor activity. An imaging study was probably ordered before the neurologist arrives; it is usually unrevealing. The EEG is the relevant test, and it should be ordered as soon as possible. Although the EEG may be disorganized, with the diffuse slowing compatable with a depressed state of consciousness, it reveal a picture consistent with NCSE. Prompt treatment may lead to improvement, although the extent of recovery depends on the extent of any underlying cerebral damage.
Elderly persons with multisystem disease, such as hepatic and renal failure, old strokes, electrolyte disturbances, and perhaps superimposed infection, are obviously quite ill and nearly always have a decline in their level of consciousness on these bases alone. It is unusual for the treating physician to consider any other cause for the mental status change. Nonetheless, NCSE may have intervened without obvious clinical evidence to suggest its diagnosis. As the patient begins to stabilize, and there is little change in mental status, the clinician may well call for a neurologic consultation. On examination, the patient will have a depressed state of consciousness ranging from lethargy to coma. Minor motor manifestations, such as myoclonic jerks or intermittent nystagmus, may be observed. Another clue to the diagnosis of NCSE may be an observation of fluctuation in the patient's level of consciousness. Usually an EEG will be ordered as part of the work-up, and NCSE may well be revealed at that time. Unfortunately, such patients present a difficult therapeutic problem. They are usually in the older age group, and this, in addition to their medical condition, makes them particularly vulnerable to the side effects of intravenous drugs. Hypotension resulting as a side effect of medication is most common (19). Moreover, it is common experience that good mental status will be difficult to support as long as the underlying medical problems continue or are unstable (20).
Nonconvulsive status epilepticus (NCSE). Note the synchronous, quite rhythmic 3 to 4 Hz sharp waves with a bifrontal preponderance. Breaks in rhythmicity occur during the first 3 and last few seconds. Some background activity is visible, and there is no lateralization.
EEG findings in NCSE are quite variable and, to the uninitiated, not always obvious. The principal feature is a generalized, usually rhythmic waveform with a bifrontal amplitude preponderance (21,22). In its most obvious form, the discharge is a high-voltage rhythmic sharp wave or spike. The configuration may be mono, bi-, or even triphasic (Figures 8.1 and 8.2). In fact, differentiation from the triphasic waves of hepatic encephalopathy may be difficult. Rhythmicity usually varies; quite regular runs alternate with more irregular sequences. Random focal or multifocal sharp wave or spike discharges may occur but often are absent. In some cases, a clue to the epileptic nature of the EEG picture is the cessation of the discharges for a brief period, during which a relatively low-voltage back ground, perhaps consisting of theta frequencies, is revealed. Such a sequence is usually not a feature of metabolic encephalopathies.
In other cases, the discharges are not so apparent. For example, a common finding is a bifrontal slow frequency in the delta range that displays a sharp contour. The slow waves are rhythmic or quasi-rhythmic in character and indeed have the same significance as the more obvious sharp potentials. The feature that strongly suggests the diagnosis is rhyth-micity, and the sharp contour to the waveform also raises suspicion. Still other patients display high-voltage paroxysms of slow or sharp activity that are frequent but not necessarily highly rhythmic. In these cases, the EEG picture, while not typical of NCSE, suggests that an epileptic contribution to the patient's depressed mental status is likely.
In this case of NCSE, the synchronous, rhythmic discharges look very much like the bi- and triphasic potentials associated with a metabolic encephalopathy.
Ideally, when the EEG shows a picture consistent with NCSE, immediately treatment with an intravenous agent should be administered under EEG control. Probably the most useful drug is lorazepam. In our laboratory, we usually give a small dose to start, either 0.5 mg or 1.0 mg IV. In many cases, a decrease in discharge frequency and rhythmicity may be observed within 2 to 3 minutes. We then may follow with a second small dose. The idea is to suppress the discharges with as little of the benzodiazepine as possible, to avoid putting the patient to sleep. This is not always possible, but we have found this a safe and often effective way to proceed. Others recommend giving valproate intravenously, which also may be effective. As mentioned above, when patients are medically unstable, it may be difficult to suppress the epilepti-form activity. In such cases, we recommend that the patient not be treated vigorously, as in cases of generalized convulsive status epilepticus. Morbidity from the treatment itself may well outweigh the benefits of discharge suppression.
1. Hauser WA. Seizure disorders: the changes with age. Epilepsia 1992;33 (Suppl 4):S6-S14.
2. So EL, Annegers JF, Hauser WA, O'Brien PC, Whisnant JP. Population-based study of seizure disorders after cerebral infarction. Neurology 1996;46:350-55.
3. Bladin CF, Alexandrow AV, Bellavance A, Bornstein N, Chambers B, Cote R, Lebrun L, Pirisi A, Norris JW. Seizures after stroke: a prospective multicenter study. Arch Neurol 2000;11:1617-22.
4. Menninger JA. Assessment and treatment of alcoholism and substance-related disorders in the elderly. Bull Menninger Clin 2002;66:166-83.
5. Beresford R, Blow F, Brower K, Singer K. Screening for alcoholism. Preventive Med 1988;17:653-63.
6. Meissner I, Wiebers DO, Swanson JW, O'Fallon WM. The natural history of drop attacks. Neurology 1986;36:1029-34.
7. Ziegler DK, Lin J, Bayer WL. Convulsive syncope: relationship to cerebral ischemia. Trans AM Neurol Assoc 1978;103:150.
8. Pavri BB, Ho RT. Syncope. Identifying cardiac causes in older patients. Geriatrics 2003;58:26-31.
9. Aminoff MJ, Scheinman MM, Griffin JC, Herre JM. Electrocere-bral accompaniments of syncope associated with malignant ventricular arrhythmias. Ann Intern Med 1988;108:791-96.
10. Rowan AJ, Dane S, Price H, Scarpa J, Sauna P, Nemire R, Ramsay RE. A pilot epidemiologic study of long-stay elderly patients with seizures. Epilepsia 1994;35 (Suppl 8):111.
11. Rosenbaum DH, Siegel M, Barr WB, Rowan AJ. Epileptic aphasia. Neurology 1986;36:281-84.
12. Fisher CM, Adams RD. Transient global amnesia. Trans Am Neurol Assoc 1958;83:143-46.
13. Caplan LR. Transient global amnesia. In: Vinken P, Bruyn G, Klawans H (eds.). Handbook of Clinical Neurology. Amsterdam: Elsevier, 1985;205-18.
14. Lewis SL. Aetiology of transient global amnesia. Lancet 1998; 352:397-99.
15. Markand ON. Electroencephalography in diffuse encephalopathies. J Clin Neurophysiol 1984;1:357-407.
16. Westmoreland BF, Saunders MG. The EEG in the evaluation of disorders affecting the brain diffusely. In: Klass DW, Daly D (eds.). Current Practice of Clinical Electroencephalography. New York: Raven Press, 1979;307-42.
17. Vestel RE, Cusack BJ. Pharmacology and aging. In: Schneider EL, Rowe JW (eds.). Handbook of the Biology of Aging (3rd ed.). San Diego: Academic Press, 1990, 349.
18. Salman C, Shader RI, Greenblatt DJ, et al. Long-versus short half-life benzodiazepines in the elderly: kinetics and clinical effects of diazepam and oxazepam. Arch Gen Psychiatry 1983; 40:293.
19. Kaplan PW. Assessing the outcomes in patients with nonconvul-sive status epilepticus: non-convulsive status epilepticus is under-diagnosed, potentially over treated, and confounded by comorbidity. J Clin Neurophysiol 1999;16:341-52.
20. Kaplan PW. Prognosis in nonconvulsive status epilepticus. Epileptic Disord 2000;2:185-93.
21. Privitera M, Hoffman M, Moore J, Jester D. EEG detection of nontonic-clonic status epilepticus in patients with altered consciousness. Epilepsy Res 1994;18:155-66.
22. Granner MA, Lee SI. Nonconvulsive status epilepticus: EEG analysis in a large series. Epilepsia 1994;35:42-47.
This Page Intentionally Left Blank
Migraine and Epilepsy
Was this article helpful?