epilepsy and loss of consciousness

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EPILEPSY AND LOSS OF CONSCIOUSNESS

EPILEPSY

'Seizure' means a convulsion or other transient event caused by a paroxysmaldischarge of cerebral neurones. Epilepsy is the continuing tendency to have seizures,

even if a long interval separates attacks. A generalized convulsion ( grand mal fit ) is

the most common recognized event.

Epilepsy is common. Its prevalence is 5 times higher in developing than developed(0.5%) countries, and the incidence is doubled. Over 2% of the population in

developed countries has two or more seizures during their lives; in 0.5% epilepsy is

an active problem. The lifetime risk of having a single seizure is 5%. Often no clear

cause is found for seizures.

Mechanisms and definitions

Spread of electrical activity between neurones is normally restricted and synchronous

discharge of neurones takes place in confined groups, producing normal EEG

rhythms. During a seizure, large groups of neurones are activated repetitively,

unrestrictedly and hypersynchronously; synaptic inhibition between them fails. High-

voltage spike-and-wave activity is the result, epilepsy's EEG hallmark .A partial seizure is epileptic activity confined to one area of cortex with a

recognizable clinical pattern. This activity either remains focal or spreads to generateepileptic activity in both hemispheres and thus a generalized seizure. This spread is

called secondary generalization. The focal nature of a seizure may not be apparentclinically because of rapid secondary generalization - an apparent generalized tonic-

clonic seizure may either have started as a focal seizure or be a primary generalizedconvulsion. Brain becomes epileptogenic either because neurones are predisposed to

be hyperexcitable, or because they acquire this tendency.

Aura means a stereotyped perception caused by initial focal electrical events

before a partial seizure, such as a smell, tingling in one limb, or strange recognizable

inner feelings.

Seizure threshold Each person has a seizure threshold. It is a concept, not a

measurement

.

Classification : here attacks are described by clinical pattern:

y G eneralized means bilateral abnormal electrical activity, with bilateral motor

manifestations and impaired consciousness.

y A partial (focal) seizure means the electrical abnormality is localized to one

part of the brain:

o (a) Simple - without loss of awareness, e.g. Jacksonian seizure.

o (b) Complex - with loss of awareness, e.g. a temporal lobe attack.

Table 21-32. The commoner types of seizure

1. Generalized seizure types

Absence seizures(a) Typical absences with 3 Hz spike-and-wave discharge (petit mal)

(b) Atypical absences with other EEG changes

Generalized tonic-clonic seizures (grand mal)

Myoclonic seizures

Tonic seizures

Akinetic seizures

2. Partial seizure types



Simple partial seizures.

Complex partial seizures.

Partial seizures evolving to tonic-clonic seizures.

Apparent generalized tonic-clonic seizures, with EEG but not clinical

evidence of focal onset

3. Unclassifiable seizures that do not fit a category above

Generalized seizure types

y Typical absence seizures (petit mal)

This generalized epilepsy almost invariably begins in childhood . Each attack isaccompanied by 3 Hz spike-and-wave EEG activity .Activity ceases, the patient

stares and pales slightly for a few seconds. The eyelids twitch; a few muscle jerks

may occur. After an attack, normal activity is resumed. Typical absence attacks are

never due to acquired lesions such as tumours. They are a developmental

abnormality of neuronal control. These children tend to develop generalized tonic-

clonic seizures in adult life (known as primary generalized epilepsy). Petit mal

describes these 3 Hz absence seizures only; clinically similar episodes can also be

produced by temporal lobe foci (partial seizures), a source of confusion.y Generalized tonic-clonic seizures (GTCS, grand mal seizures)

Following a vague warning, the tonic phase commences. The body becomes rigid,

for up to a minute. The patient utters a cry and falls, The tongue is usually bitten.There may be incontinence of urine or faeces.

The clonic phase then begins, with generalized convulsing, frothing at the mouth and bilateral, rhythmic jerking of muscles. This lasts from a few seconds to several

minutes. Seizures are usually self-limiting, followed by drowsiness, confusion or

coma for several hours.

y Myoclonic, tonic and akinetic seizures1. M yoclonic seizures describe isolated muscle jerking. J uvenile myoclonic

epilepsy is one variety, seen in adolescence.

2. Tonic means intense stiffening of the body, not followed by jerking.

3. Akinetic means cessation of movement, falling and loss of consciousness.

EPILEPSY: ETIOLOGICAL FACTORS

1. Genetic predisposition< 2%.

2. Developmental, e.g. hamartomas, neuronal migration abnormalities

3. Hippocampal sclerosis

4. Brain trauma and surgery 2%.

5. Pyrexia

6. Intracranial mass lesions, e.g. tumour 6%, neurocysticercosis.

7. Vascular, e.g. cerebral infarction< 15%., AVM

8.

Encephalitis and inflammatory conditions, e.g. herpes simplex, in MS×3than general population.

9. Metabolic abnormalities, e.g. porphyria, hypocalcaemia

10. Neural degenerative disorders, e.g. Alzheimer's

11. Provoked seizures, e.g. photosensitivity, sleep deprivation

12. Drugs, e.g. cyclosporine, Lidocaine, quinolones, SSRIs, interferon, cocaine,

lithium, withdrawal of amphetamines, barbiturates, Alcohol-related seizures

for 6%.



Partial seizure types

y Simple partial seizures (e.g., Jacksonian seizures)

Jerking typically begins on one side of the mouth or in one hand, sometimes

spreading to involve the entire side. This visible spread of activity is called the march

of a seizure. With a frontal lesion, conjugate gaze deviates away from the

epileptic focus and the head turns; this is known as an Adversive seizure. Localtemporary paralysis of the limbs affected sometimes follows - Todd's paralysis.

y Temporal lobe seizures

These partial seizures can produce feelings of unreality (jamais vu) or undue

familiarity (déjà vu) with the surroundings. Blank episodes of staring, vertigo, visual

hallucinations.

Etiology and precipitants

A cause is found in <1/3 of patients:

Neurocysticercosis is a major cause of epilepsy where cysticercosis is endemic.

1. Genetic predisposition and developmental anomalies

Over 200 genetic disorders. About 30% of epilepsy patients have first-degree relativeswith seizures. Usually the mode of inheritance is uncertain. A low seizure threshold

seems to run in some families. Petit mal and other primary generalized epilepsies are

often inherited as an autosomal dominant trait with variable penetrance. Primaryepilepsies are due to complex developmental abnormalities of neuronal control; there

are abnormalities in synaptic connections, and anomalies in neurotransmitter distribution and release. Neuronal migration defects in utero, dysplastic areas of

cerebral cortex and hamartomas contribute to seizures both in infancy and adult life.

2. Trauma, hypoxia and surgery

Perinatal trauma (cerebral contusion and haemorrhage) and fetal anoxia are causes of childhood seizures. Hypoxic damage in childhood to the hippocampi leads to

Hippocampal sclerosis, another prominent cause. Brain injury is sometimes followed

by seizures within the first week (early epilepsy) or many months or years later(late epilepsy). To cause epilepsy, the injury must (usually) be sufficient to cause

coma. Early epilepsy, a depressed skull fracture, penetrating brain injury, cerebral

contusion, dural tear or intracranial haematoma increase the incidence of late post-

traumatic epilepsy.

Brain surgery is followed by seizures in 3-5%.

Brain tumours (and abscesses), Mass lesions in the cortex cause epilepsy - either

partial or secondary generalized seizures. If epilepsy develops in adult life, the chance

of finding an unsuspected tumour is around 3%.

Hydrocephalus also lowers seizure threshold.

3. Vascular and degenerative brain disorders

There is a peak in incidence late in life.

4. Encephalitis and inflammatory conditionsSeizures are frequent features of encephalitis, cerebral abscess, tuberculoma, cortical

venous thrombosis and neurosyphilis. They also occur in chronic meningitis (e.g. TB)

and may rarely be the first sign of acute bacterial meningitis. Neurocysticercosis is a

prominent cause of seizures in countries where the pork tapeworm is endemic, e.g.

India, South America, and is a major public health problem.

5. Alcohol and drugs

Either while drinking heavily, during periods of withdrawal or Alcohol-induced

hypoglycemia also provokes attacks.



Phenothiazines, MAO inhibitors, TCAs, SSRIs, amphetamines, Lidocaine, propofoland nalidixic acid sometimes provoke fits, either in overdose or at therapeutic

doses in individuals with a low seizure threshold.

Withdrawal of antiepileptic drugs (especially phenobarbital) and

benzodiazepines may provoke seizures.

6. Metabolic abnormalities

Seizures can follow:

y Hypocalcaemia, hypoglycemia, hyponatremia

y Acute hypoxia

y Uraemia, hepatocellular failure

y Mitochondrial disease, porphyria.

7. Provoked seizures: photosensitivity, pyrexia

Photosensitivity may be recorded on occipital EEG electrodes. High pyrexia can

provoke convulsions in children under 5 years (febrile convulsions). In most, there is

no recurrence; febrile convulsions are not labeled as epilepsy.

Sleep deprivation can be a cause.

.

Diagnosis

Neurological examination may be normal or point to a clinical diagnosis. General

screening, including serum calcium, and an ECG (rhythm, conduction abnormalities,

and QT interval) should be done.

y Electroencephalography

EEG is a useful test, despite limitations. It is usually performed following a first fit,though the therapeutic yield is low.

y During a seizure the EEG is almost invariably abnormal, because spikes

reach electrodes overlying brain.

y EEG evidence of seizure activity is shown typically by focal cortical spikes or by generalized spike-and-wave activity. Epileptic activity is continuous

in status epilepticus.

y 3 Hz spike-and-wave occurs specifically in petit mal always during an attack

and frequently in between them.

y A normal EEG between attacks (interictal) does not exclude epilepsy; many

people with epilepsy have normal interictal EEGs.y An abnormal interictal EEG does not prove that a particular attack was

epileptic.y EEG videotelemetry is vital for studying attacks of uncertain nature (e.g. non-

epileptic attacks

y CT and/or MR imaging is indicated in all new cases.

Treatment

Emergency measures

Reduce harm and maintain both during a prolonged seizure and in Postictal coma.

A prolonged seizure (longer than 3 minutes) or repeated seizures are treated withrectal (10 mg) or i.v. diazepam or midazolam. If there is any suspicion of

hypoglycemia, take blood for glucose and give i.v. glucose. Serial epilepsy describesrepeated seizures with brief periods of recovery. These may lead to status



epilepticus. Sudden death in a seizure is unusual but does occur.

Status epilepticusThis medical emergency means continuous seizures without recovery of

consciousness. It consists of prolonged serial seizures (two or more) occurring with

incomplete recovery of consciousness. Status epilepticus has a mortality of 10-15%.

Over 50% of cases occur without a previous history of epilepsy. Some 25% with

apparent refractory status have p seudostatus (non-epileptic attack disorder );iatrogenic errors and morbidity are significant.

Not all status is convulsive. In absence status, for example, status is non-convulsive -the patient is in a continuous, distant, stuporose state. E pilepsia partialis continua are

continuous seizure activity in one part of the body, such as a finger or a limb,without loss of consciousness. This is often due to a cortical neoplasm or, in the

elderly, a cortical infarct.

Practical Box 21.4 Status epilepticus - management Of prime

importance:

y Treat convulsions quickly.

y Accuracy of diagnosis.

y Continued ITU monitoring and cardiorespiratory support.

Several treatment schedules exist:

y At home, give immediate diazepam 10-20 mg i.v. at 5

mg/min and repeat once. If i.v. access is impossible, give

rectal diazepam or paraldehyde

y Arrange immediate admission

y Administer oxygen, monitor ECG, BP, routine bloods

(include alcohol, sugar, calcium, magnesium, drug screen,

anticonvulsant levels)

y Give thiamin i.v. (250 mg) if nutrition is poor or alcoholabuse suspected. (In the UK, give vitamin B and C, high-

potency ampoules, one pair i.v. over 10 mins)

y Antiepileptic drugs (AEDs):

Give Lorazepam 4 mg i.v at 2mg/min.

Reinstate previous AEDs, measure levels urgently. Has

the patient had phenytoin recently?

if status continues, i.v. phenytoin or fosphenytoin is

used.(phenytoin 15mg/kg i.v diluted to 10mg/ml in 0.9%

saline into a large vein at < 50mg/min-5ml ampule

contains 250mg of phenytoin). Fosphenytoin is a prodrug

of phenytoin and can be given faster, doses are expressedin phenytoin equivalents (P.E): fosphenytoin 1.5mg =

1mg phenytoin.

Give 5mg/kg (P.E) fosphenytoin (15mg×1.5 =22.5mg)diluted

to 10mg/ml in 0.9%saline at 50-100mg(P.E)/min.

If status continues, give phenobarbital 10 mg/kg diluted 1 in

10 in water for injection at <100 mg/min. (Phenobarbital 200



mg/mL 1 mL vial in propylene glycol 90% with water for injection 10%.) Intravenous clonazepam, paraldehyde and

clomethiazole are also used If status persists >90 minutes, use thiopental or propofol

anaesthesia with assisted ventilation

y EEG monitoring is valuable if there is doubt about the natureof status

y CT may reveal an underlying cause

y Remember: 25% of apparent status turns out to be

pseudostatus

y Remember: potential unwanted effects of drugs, e.g.

hypotension, cardiorespiratory arrest, and the need for

continuous monitoring

Antiepileptic drugs (AEDs)

AEDs are indicated when there is a firm clinical diagnosis of epilepsy and a

substantial risk of recurrent seizures. AED use carries the stigma of epilepsy. For both partial and generalized seizures, monotherapy with an established first-line AED isthe initial choice. Doses should start low and be increased until control is achieved or

tolerance exceeded. If control is not achieved, a second drug is added. There remaindifferent views about the most appropriate drugs for each seizure type.

Drug levels.Serum levels of all AEDs can be measured. With phenytoin the therapeutic range is

well defined and the level should usually be monitored every few months Monitoring

serum levels of other AEDs are less useful. Levels are not usually measured routinely

unless compliance or toxicity is an issue.

Unwanted effects of drugs.

Intoxication with all AEDs causes ataxia, nystagmus and dysarthria. Chronic

phenytoin causes gum hypertrophy, Hypertrichosis, osteomalacia, folate deficiency, polyneuropathy and encephalopathy. A wide range of potential unwanted effects are

known. See Table 21.36 for some serious idiosyncratic (i.e. non-dose-related) side-

effects. The majority of severe skin reactions (e.g. toxic epidermal necrolysis)

following phenytoin, carbamazepine, valproate and phenobarbital occur within the

first 8 weeks of treatment.Two drugs rarely commenced outside a specialist centre are phenobarbital and its

derivative primidone (drowsiness, cognitive impairment), though phenobarbital stillhas a place in status. Vigabatrin can cause irreversible visual field defects and is no

longer advocated.

Refractory epilepsy

Despite therapy, seizures persist in some 20-35% of cases. Rigorous attention to

diagnosis, to concordance (compliance) and to trials of different drugs can sometimesreduce seizure frequency. Many cases of refractory seizures are treated in specialistunits: the question of surgery can be reviewed.

Epilepsy in the elderly

25% of new cases of epilepsy develop over the age of 65. Many patients have CVAs,

neurodegenerative conditions or brain tumours. The onset of seizures commonly

leads to loss of independence and to physical injuries with their complications (e.g.

fractures, subdural haematoma). With adequate AEDs, seizure control can be

achieved in some 70% of this vulnerable population.



Women, epilepsy, pregnancy and AEDs

y Fertility. There is some reduction of fertility in women with

epilepsy. This is multifactorial. 1/3 of women with epilepsy havesome ovarian abnormality: irregular menstrual cycles,

anovulatory cycles and polycystic ovaries, more frequent in patients taking valproate.

y Birth defects.Table 21-34. Principal antiepileptic drugs and common seizure types

Generalized tonic-

clonic seizures (grand

mal) and partial

Petit mal Myoclonic Atypical absence,

tonic and

akinetic

First-line Carbamazepine Ethosuximide Valproate Valproate

Lamotrigine Valproate Clonazepam Lamotrigine

Phenytoin Lamotrigine Clonazepam

Valproate

Second-

line and/oradd-ons

Phenobarbital Clobazam Clobazam Topiramate

Primidone Clonazepam Levetiracetam Clobazam

Levetiracetam Topiramate Topiramate Levetiracetam

Topiramate Lamotrigine Phenobarbital

Newer drugs (Table

21.35)

Acetazolamide

May

worsen

attacks

Carbamazepine Carbamazepine

Phenytoin Phenytoin

Other drugs usually initiated in specialist centres are gabapentin,oxcarbazine, tiagabine, zonisamide, Pregabalin.

Table 21-35. Antiepileptic drugs: doses and therapeutic levels

Usual adult daily dose (mg) Therapeutic range (mol/L)

Phenytoin 300-450 40-80

Carbamazepine 400-1000 20-50

Valproate 800-2000 200-700

Table 21-36. Antiepileptic drugs: some idiosyncratic unwanted effects

Drug Non-dose-related effects

Phenytoin RashesBlood dyscrasias

Lymphadenopathy

Systemic lupus erythematosus

Toxic epidermal necrolysis(TEN)

Carbamazepine Rashes

Blood dyscrasias, e.g. severe

leucopenia



Toxic epidermal necrolysis

Valproate Anorexia

Hair loss

Liver damage

Lamotrigine Toxic epidermal necrolysis

The overall risk of birth defects in babies of mothers who take one AED is around7%, higher than the 3% in the population. Counseling before conception is essential.

Some women choose to stop AEDs before becoming pregnant. If drugs are continued,monotherapy with a first-line drug is preferable with folic acid (5 mg/day)

supplement. Careful antenatal screening is required.Vitamin K 20 mg orally shouldalso be taken daily during the week before delivery to prevent neonatal

haemorrhage (caused by inhibition of vitamin K transplacental transport).

y Contraception.

AEDs that induce enzymes (e.g. carbamazepine, phenytoin and phenobarbital) reduce

efficacy of OCPs; valproate does not. A combined contraceptive pill containing

either ethinylestradiol 50 g or mestranol 50 g provides greater contraceptive

security at the risk of side-effects. An IUCD or barrier methods of contraception are

an alternative.y Breast-feeding.

Mothers are not discouraged from breast-feeding.

y Drug withdrawal

Epilepsy, when controlled, may remain in remission. AED withdrawal is sometimes

possible. Withdrawal should not usually be considered until all fits have been

absent for at least 2-3 years. Less than 50% of attempts to withdraw AEDs are

successful. The UK Driving Licensing Authority (DVLA Swansea) recommends that

patients do not drive while AEDs are being reduced and for 6 months after stopping

them.

y Neurosurgical treatmentSeveral surgical approaches are used in epilepsy. Amputation of the non-dominant

anterior temporal lobe can be performed in a patient with uncontrolled seizures andHippocampal sclerosis defined by imaging and confirmed by EEG. In these highly

selected cases (under 1% of epilepsy patients) in specialist centres this surgical

treatment is very effective, with cure rates (complete seizure cessation) over 50%.

Section of the corpus callosum and hemispherectomy are also used.

y Driving and epilepsy

Must be seizure-free for 12 months in the UK and European.

OTHER FORMS OF DISTURBED CONSCIOUSNESS

F alls must be distinguished from episodes of disturbed consciousness. The precise

cause of falls often remains ill-defined.

1. Syncope, postural hypotension and drop attacks

The simple faint is due to sudden reflex bradycardia with vasodilatation of both peripheral and splanchnic vasculature. This simple syncope (neurocardiogenic

syncope) is a common response to prolonged standing, fear, venesection or pain.Syncope almost never occurs in the recumbent posture. The subject falls to the

ground and is unconscious for less than 2 minutes. Recovery is rapid. Jerking

movements can occur. Incontinence of urine can occur. Syncope can occur in the

following conditions:

Syncope occurs after micturition in men, particularly at night, and in either sex

when the venous return to the heart is obstructed by breath-holding and severe



coughing. Effort synco pe (on exertion) is of cardiac origin.

P ostural hy potension esp. in the elderly, in autonomic neuropathy, with phenothiazines, levodopa or TCAs.

C arotid sinus problems.

S evere anaemia.

Table 21-37. Causes of sudden attacks, 'funny turns' 1. Epilepsy, Non-epileptic attacks (pseudoseizures).

2. Cataplexy, narcolepsy, sleep paralysis

3. Syncope

4. Simple faints, Panic attacks, Hyperventilation, Breath-

holding

5. Cardiac dysrhythmias

6. Cough syncope, Effort syncope, Micturition syncope,Carotid sinus syncope.

7. Autonomic failure

8. Basilar migraine

9. Choking attacks, apnoeic episodes

10. Transient ischaemic attacks

11. Drop attacks, Hydrocephalic attacks, Tonic attacks(MS).

12. Hypoglycaemia, Hypocalcaemia.

13. Severe vertigo

14. Night terrors in children

15. Drug reactions (e.g. oculogyric crises) hereConsciousness is preserved.

16. Paroxysmal dyskinesias

17. Carcinoid syndrome, scombroid poisoning

18. Phaeochromocytoma

Drop attacks are instant, unexpected episodes of lower limb weakness with falling,

largely in women over 60 years. Awareness is preserved. They are due to suddenchange in lower limb tone, presumably of brainstem origin, rather than

thromboembolism. Sudden attacks of leg weakness also occur in hydrocephalus.

T ransient cerebral (posterior circulation) ischaemia rarely leads to loss of

consciousness; patients sometimes faint during a severe basilar migraine.

Syncope: investigation and management

Distinguish from epilepsy on clinical grounds. Persistent jerking movements

and post-episode confusion with amnesia are suggestive of a fit, and unusual

in a faint.

Cardiac monitoring is used to detect dysrhythmia. Tilt testing is sometimes diagnostic, but has low sensitivity.

The immediate management of syncope, or impending syncope, is to lay the patient

down, lift the legs and record the pulse. In rare circumstances where brain blood flow

cannot be restored, brain infarction can follow syncope.

1. Non-epileptic attacks (pseudoseizures)Usually there are bizarre limb movements. EEG videotelemetry is valuable. The



serum prolactin level is of some value: this rises during a grand mal seizure but not during a pseudoseizure (or a partial seizure).

2. Panic attacksAre usually associated with autonomic disturbances such as tachycardia, sweating

and piloerection. Consciousness is usually preserved and attacks easily recognized.

3. Hyperventilation

Is common and overbreathing causes alkalosis. This leads to dizziness, anxiety andsometimes circumoral/peripheral tingling and tetany, e.g. carpopedal spasm.

Occasionally there is loss of consciousness.

4. Breath-holding attacks

Occur in children.

5. Hypoglycaemia

Causes attacks of loss of consciousness, sometimes with a convulsion. There is often

warning, with hunger, malaise, shaking and sweating. Prompt recovery occurs with

glucose, or household sugar. Prolonged hypoglycemia causes widespread cerebral

damage. Hypoglycaemic attacks unrelated to diabetes are rare. Feeling faint after

fasting does not indicate anything serious.

6. Hypocalcaemia

May be accompanied by a grand mal fit as seizure threshold is lowered.7. Vertigo.

When acute & severe as to cause prostration: a few seconds' unconsciousnesssometimes follows.

8. ChokingIn partial obstruction it causes intense coughing and laryngeal spasm. In complete

obstruction, the person becomes blue and silent. Death may follow.

9. Carcinoid syndrome, phaeochromocytoma and scombroid poisoning

Flushing and palpitation is sometimes mistaken for anxiety, allergy or possibly a

partial seizure.

SLEEP AND ITS DISTURBANCES

Sleep is required to preserve recent memory

refresh emotional equilibrium Avoid neurotransmitter depletion.

In insomnia, sleep is fitful, Less time than usual is spent in REM sleep. In old age,

sleep requirement falls, sometimes to 4 hours a night. Insomnia is rarely a feature of

neurological disease.

Seizures may occur predominantly or solely during sleep. Sleepwalking, jerking

episodes and movements in sleep are events seen in the normal population and are

not suggestive of brain pathology.

Narcolepsy and cataplexy

N arcoleptic attacks are periods of irresistible sleep, i.e. excessive daytimedrowsiness, in inappropriate circumstances. Episodes occur when there is little

distraction, after meals, while travelling in a vehicle, or sometimes without obvious

cause. N arcole p sy is strongly associated with HLA-DR2 and HLA-DQBl*0602

antigens. Narcolepsy patients positive for these antigens may have subnormal CSF

hypocretin 1 (orexin) levels, possibly on an autoimmune basis.

C ataplexy is sudden loss of lower limb tone - falling with intact awareness. Attacks

are often set off by sudden surprise or emotion.

Narcolepsy and cataplexy sometimes coexist and are accompanied by vivid



hypnagogic hallucinations (on falling asleep) hypnopompic hallucinations (on waking)

Sleep paralysis - a frightening inability to move.Treatment (rarely with great success)

Methylphenidate, Dexamphetamine, Modafinil,

TCAs, particularly Clomipramine, are used.

Siberian ginseng ( Elenthrococcus serticosus) and St John's Wort ( Hy pericum perforatum) are also used.

10. Central sleep apnoea

This rarity is due to impairment of central ventilatory control due to brainstem

pathology. Apnoea occurs typically at the onset of sleep. It is seen in non-obese

people without the typical history of snoring seen in the more usual obstructive sleep

apnoea.

epilepsy and loss of consciousness

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