EPILEPSY AND LOSS OF CONSCIOUSNESS

EPILEPSY
'Seizure' means a convulsion or other transient event caused by a paroxysmal
discharge 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 generate
epileptic activity in both hemispheres and thus a generalized seizure. This spread is
called secondary generalization. The focal nature of a seizure may not be apparent
clinically because of rapid secondary generalization - an apparent generalized tonic-
clonic seizure may either have started as a focal seizure or be a primary generalized
convulsion. 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:
 Generalized means bilateral abnormal electrical activity, with bilateral motor
manifestations and impaired consciousness.
 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
 Typical absence seizures (petit mal)
This generalized epilepsy almost invariably begins in childhood. Each attack is
accompanied 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.
 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.
 Myoclonic, tonic and akinetic seizures
1. Myoclonic seizures describe isolated muscle jerking. Juvenile 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. tumour6%, neurocysticercosis.
7. Vascular, e.g. cerebral infarction< 15%., AVM
8. Encephalitis and inflammatory conditions, e.g. herpes simplex, in MS×3
than 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

 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. Local
temporary paralysis of the limbs affected sometimes follows - Todd's paralysis.
 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 relatives
with 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. Primary
epilepsies 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 conditions
Seizures 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, propofol
and 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:

 Hypocalcaemia, hypoglycemia, hyponatremia

 Acute hypoxia
 Uraemia, hepatocellular failure
 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.
 Electroencephalography
EEG is a useful test, despite limitations. It is usually performed following a first fit,
though the therapeutic yield is low.

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

reach electrodes overlying brain.
 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.
 3 Hz spike-and-wave occurs specifically in petit mal always during an attack
and frequently in between them.
 A normal EEG between attacks (interictal) does not exclude epilepsy; many
people with epilepsy have normal interictal EEGs.
 An abnormal interictal EEG does not prove that a particular attack was
epileptic.
 EEG videotelemetry is vital for studying attacks of uncertain nature (e.g. non-
epileptic attacks

 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 with
rectal (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 describes
repeated seizures with brief periods of recovery. These may lead to status
epilepticus. Sudden death in a seizure is unusual but does occur.
Status epilepticus
This 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 pseudostatus (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. Epilepsia 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:

 Treat convulsions quickly.

 Accuracy of diagnosis.
 Continued ITU monitoring and cardiorespiratory support.

Several treatment schedules exist:

 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
 Arrange immediate admission
 Administer oxygen, monitor ECG, BP, routine bloods
(include alcohol, sugar, calcium, magnesium, drug screen,
anticonvulsant levels)
 Give thiamin i.v. (250 mg) if nutrition is poor or alcohol
abuse suspected. (In the UK, give vitamin B and C, high-
potency ampoules, one pair i.v. over 10 mins)
 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 expressed in
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

 EEG monitoring is valuable if there is doubt about the nature

of status
 CT may reveal an underlying cause
 Remember: 25% of apparent status turns out to be
pseudostatus
 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 is
the 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 remain
different 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 still
has 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 sometimes
reduce seizure frequency. Many cases of refractory seizures are treated in specialist
units: 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
 Fertility. There is some reduction of fertility in women with
epilepsy. This is multifactorial. 1/3 of women with epilepsy have
some ovarian abnormality: irregular menstrual cycles,
anovulatory cycles and polycystic ovaries, more frequent in
patients taking valproate.
 Birth defects.
Table 21-34. Principal antiepileptic drugs and common seizure types
  Generalized tonic- Petit mal Myoclonic Atypical absence,
clonic seizures (grand tonic and
mal) and partial akinetic

First-line Carbamazepine Ethosuximide Valproate Valproate

  Lamotrigine Valproate Clonazepam Lamotrigine

  Phenytoin   Lamotrigine Clonazepam

  Valproate      

Second- Phenobarbital Clobazam Clobazam Topiramate

line and/or
add-ons

  Primidone Clonazepam Levetiracetam Clobazam

  Levetiracetam Topiramate Topiramate Levetiracetam

  Topiramate Lamotrigine   Phenobarbital

  Newer drugs (Table     Acetazolamide

21.35)

May   Carbamazepin Carbamazepin  

worsen e e
attacks
    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 (μmol/L)

Phenytoin 300-450 40-80

Carbamazepin 400-1000 20-50

e

Valproate 800-2000 200-700

Table 21-36. Antiepileptic drugs: some idiosyncratic unwanted effects
Drug Non-dose-related effects
Phenytoin Rashes
  Blood 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 around
7%, 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 should
also be taken daily during the week before delivery to prevent neonatal
haemorrhage (caused by inhibition of vitamin K transplacental transport).
 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 μg or mestranol 50 μg provides greater contraceptive
security at the risk of side-effects. An IUCD or barrier methods of contraception are
an alternative.
 Breast-feeding.
Mothers are not discouraged from breast-feeding.
 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.
 Neurosurgical treatment
Several surgical approaches are used in epilepsy. Amputation of the non-dominant
anterior temporal lobe can be performed in a patient with uncontrolled seizures and
Hippocampal 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.
 Driving and epilepsy
Must be seizure-free for 12 months in the UK and European.
OTHER FORMS OF DISTURBED CONSCIOUSNESS
Falls 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 syncope (on exertion) is of cardiac origin.
 Postural hypotension esp. in the elderly, in autonomic neuropathy, with
phenothiazines, levodopa or TCAs.
 Carotid sinus problems.
 Severe 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) here
Consciousness 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 sudden
change in lower limb tone, presumably of brainstem origin, rather than
thromboembolism. Sudden attacks of leg weakness also occur in hydrocephalus.
Transient 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 attacks
Are 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 and
sometimes 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' unconsciousness
sometimes follows.
8. Choking
In 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
Narcoleptic attacks are periods of irresistible sleep, i.e. excessive daytime
drowsiness, in inappropriate circumstances. Episodes occur when there is little
distraction, after meals, while travelling in a vehicle, or sometimes without obvious
cause. Narcolepsy 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.
Cataplexy 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 (Hypericum
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.