24 ORGANIC PSYCHIATRY Ng Beng Yeong Introduction

Organic brain syndrome includes those psychiatric disorders that are caused by

cerebral disorder or dysfunction. In the context of the Tenth Revision of the International Classification of Diseases and Related Health Problems (ICD-10), the term organic implies that a syndrome so classified can be attributed to an independently diagnosable cerebral or systemic disease. Generally there is a clear temporal association between onset of brain pathology and development of the disorder.

Organic psychosis is suspected when there is a neurological deficit producing an

altered mental state, which is suggested by altered consciousness, fluctuating level of consciousness, memory problems, visual, olfactory, somatic and gustatory hallucinations and/or sphincter disturbance. Visual hallucinations, for instance, can be encountered in the following conditions: ocular disorders (e.g. macular degeneration, cataracts), optic nerve and tract disorders, midbrain lesions (e.g. stroke, tumors), geniculocalcarine radiation lesions, occipital or temporal lesions (e.g., stroke, tumours, seizures), migraine, narcolepsy, Alzheimers disease, cortical Lewy body disease, Parkinsons disease after dopaminergic treatment, drug intoxication or withdrawal, metabolic encephalopathies, schizophrenia, depression or mania with mood-congruent hallucinations (Cummings & Trimble, 1995). Paranoid symptoms have been mentioned traditionally in Huntingtons disease and grandiosity is commonly described in neurosyphilis and sometimes in Picks disease, due to predominantly pre-frontal lobe involvement at certain stages of these illnesses.

Organic mental disorders have known biological causes and pathophysiological

mechanisms but the boundary between organic and functional disorders shifts over time, both within the field of psychiatry and for particular patients. Historically, mental disorders (e.g. general paresis of the insane) have been reclassified as organic if a specific underlying brain dysfunction could be identified. For an individual patient, a depressive episode may turn out to be an early manifestation of an underlying neurological condition (e.g. Huntingtons chorea), and the person may be more appropriately diagnosed to have an organic mood disorder. Psychiatric disorders are more likely to develop in vulnerable individuals as a result of the interaction between the persons, the stressful situation and the social and emotional supports available. To illustrate, the stress of physical illness, cognitive impairments and the patients premorbid personality may bring about affective changes. Table 1 lists the neurologic disorders associated with mania or hypomania. Premorbid personality may determine a persons reaction to illness and disability while psychosocial effects may impact on the nature and severity of anxiety and depression and the ability of patient to compensate for his/her cognitive deficits.

1

Table 1. Neurologic Disorders Associated with Mania or Hypomania

Stroke (most common with right-brain lesions and in patients with a family history of psychiatric illness)

Parkinsons disease after dopaminergic therapy Huntingtons disease Idiopathic basal ganglia calcification Traumatic brain injury Epilepsy (peri-ictal) Frontotemporal dementias General paresis (syphilitic encephalitis)

The most important clinical clues to possible underlying organic disease are often in the mental state examination. Organic hallucinations are usually visual, coloured, moving and often show size distortion. They are more troublesome in the evening. Organic delusions are poorly elaborated, not well sustained and lack emotional intensity. A brief cognitive examination is an essential part of the routine assessment of all psychiatric patients. A detailed one is indicated where history, presentation or the nature of their complaint (e.g. epilepsy, head injury, stroke, brain tumours, delirium) make cognitive impairment likely. Higher function can be examined using relatively simple tests while mental state is examined using observation of the patient and attention to points within the history. Bedside Cognitive Testing The following steps are hereby suggested: 1. Assess level of consciousness (coma to alert wakefulness). 2. Observe and assess orientation for time, place and person. Time disorientation is

often the first sign of an acute organic state. 3. Assess attention and vigilance (digit repetition, serial 7 subtraction, digit reversal,

days or months in reverse order). Attention span may be assessed by having the patient repeat a list of words or a digit sequence presented at the rate of one digit per second. Intact repetition of six digits forward rules out major attentional disturbance. Inability to repeat at least five digits is considered abnormal. The serial sevens test is done by asking the patient to take sevens away from a hundred until he gets down to nought, going as quickly as he reasonably can without making mistakes.

2

4. Assess verbal output (e.g. spontaneous speech during conversation). Language functions are primarily served by the dominant (left) hemisphere.

5. Ask patient to point to objects in the room/ward named by the examiner. This

examines language function associated with the dominant temporoparietal region. 6. Ask patient to name objects, body parts, and colours. Dysnomia can be the product

of a dominant temporal or dominant parietal lesion. 7. Test memory ability to remember 3 items or using the name and address test. 8. Test general knowledge for recent events and knowledge for remote events. 9. Test for constructional ability (e.g. copy circle, cross, and cube; draw a clock), which

is subserved by the non-dominant parietal lobe. 10. Test for ideomotor and ideational apraxia. Patient can be asked to perform simple

commands (e.g. to demonstrate the use of imagined household items like a toothbrush or comb). In ideomotor apraxia the patient is unable to carry out a motor act when asked, but is able to do so in circumstances where the response is more automated. For instance, he is unable to wave goodbye when asked, but can do so when a relative leaves the ward. The commonest site for a lesion seems to be in the dominant parietal lobe. Ideational apraxia refers to a difficulty in organizing more complex sequences of voluntary actions, such as using a match to light a cigarette. The lesion is usually of the dominant parietal lobe, but the condition is mostly associated with diffuse brain damage.

11. Test executive function which refers to those abilities to initiate, organize, direct,

monitor and evaluate oneself (e.g. verbal fluency: number of animals named in 1 minute or number of words that begin with a certain letter in 1 minute; perseveration: fist-edge-palm test). Perseveration is the persistence of a response when it is no longer appropriate or relevant. In the Luria three-step test the examiner demonstrates the series of hand movements fist, edge, palm five times without verbal cues, and then asks the subject to repeat the sequence. Patients with frontal deficits are unable to reproduce the movements, even if given specific verbal clues.

12. Test for right-left disorientation by asking the patient to perform several tasks, each

of which requires that he/she tell left from right twice (e.g. patient is told, Touch your right hand to your left elbow).

13. Test calculation skills by asking the patient to perform oral arithmetic calculations,

which sample the four basic operations, i.e. addition, subtraction, division, and multiplication. A dominant parietal lobe lesion may lead to the development of Gerstmanns syndrome (dysgraphia, dyscalculia, finger agnosia, and right-left disorientation).

14. Test proverb interpretation, which is commonly used for assessing thinking and

divergent reasoning. Unfortunately, responses to proverbs (sayings with broader meaning) do not correlate well with deficits in abstract thinking and are strongly influenced by culture, educational level and socioeconomic class.

3

15. Test understanding of similarities, the ability to appreciate the commonality between two objects. Low intelligence, psychosis, distraction or dementia may produce impairment in abstracting ability.

16. Retest memory: recall items of earlier memory test.

Table 2. Patterns of Focal Loss Lobe Alteration in higher function Associations

Frontal Apathy, disinhibition Contralateral hemiplegia, Brocas aphasia (dominant hemisphere), primitive reflexes

Temporal Memory Wernickes aphasia (dominant hemisphere), upper quadrantanopia

Parietal Calculation, perceptual and spatial orientation (non-dominant hemisphere)

Apraxia (dominant hemisphere), homonymous hemianopia, hemisensory disturbances, neglect

Occipital Perceptual and spatial orientation

Hemianopia

Delirium

Delirium is derived from the Latin de-, off, away from and lira, a ridge between

ploughed furrows. Literally it means off the ridge but more colloquially off the rails. It denotes disorders that are acute and potentially reversible whereas dementia tends to be chronic and progressive. Delirium is also known as acute brain syndrome, acute confusional state, acute organic brain syndrome and acute organic psychosis. ICD-10 defines it as an aetiologically non-specific syndrome, characterised by concurrent disturbances of consciousness and attention, perception, thinking, memory, psychomotor behaviour, emotion and the sleep-wake cycle. Misinterpretations, illusions and hallucinations are very common but are usually fleeting and changeable. Abnormal visual perceptions combined with faulty thinking and memory lead to disorientation in place. Two subtypes of delirium have been described: low road (characterised by sedation, coma; infrequent source of psychiatric consultation) and high road (involves agitation, behavioural disruption, hallucinations; may progress to seizures, coma, death). Common Causes of Delirium 1. Central nervous system disorders

Head injury Tumours and subdural haematoma, cerebral abscess Degenerative diseases Vascular diseases; subarachnoid haemorrhage; thrombosis; embolism Infections: meningitis, encephalitis, AIDS encephalopathy Epilpesy

4

2. Metabolic disorders Uraemia Hepatic failure Pulmonary failure Congestive cardiac failure Electrolyte imbalance Acidosis/alkalosis

3. Endocrine disorders

Hyper/hypothyroidism Hyper/hypoglycaemia Parathyroid disease Cushings disease, Addisons disease

4. Nutritional and vitamin deficiencies

Anaemia Thiamine deficiency B12 deficiency

5. Systemic infections

Pneumonia Septicaemia Urinary tract infection

6. Toxic causes

Drug intoxication (anticholinergics, hypnotics) Alcohol Heavy metals Carbon monoxide poisoning

Medications like tricyclic antidepressants, antipsychotics or neuroleptics, Benzhexol

(Artane), antihistamines and atropine may induce anticholinergic delirium. Systemic manifestations of anticholinergic side effects are dry mouth, constipation, and trouble initiating urination. Central nervous system symptoms can range from mild confusion or memory disturbance to a toxic delirium with psychotic symptoms, disorientation, blurred vision, and warm, dry, flushed skin. All these symptoms are embraced in the following mnemonic: Hot as a hare, blind as a bat, dry as a bone, red as a beet, mad as a hatter. I. Neuropsychiatric Sequaelae of Neurological Diseases Epilepsy Case History

A 25-year-old Chinese female with a known history of epilepsy reports a worsening of her seizures. The fits were very frequent and not responding to anticonvulsants. Video telemetry demonstrated that when she was supposedly unresponsive there was actually preservation of alpha rhythm on the EEG. Suspected to have non-epilpetic seizures, she was referred to a psychiatrist who diagnosed her to be suffering from dissociative states. Two main stressors were identified. First, she found her job too demanding and often had

5

problems meeting deadlines. Second, her parents have marital disputes, are not on talking terms with each other, and would rely on her to relay messages. A cognitive-behavioural approach was adopted to help patient cope with stresses better. Her parents marital disputes have reached an impasse and she was helped to come to terms with her parents failed marriage. It was a painful realisation and she needed some support. Her non-epileptic attacks eventually ceased.

There are a number of possible explanations for the over representation of behavioural disturbances among epileptic populations. Epilepsy and the psychiatric disturbances may have a shared organic basis, or the psychiatric disturbances could be a result of anti-epileptic drugs or the psychosocial effects of living with epilepsy. Psychiatric Presentations Related to the Persons Epilepsy Syndrome A. Temporally related to the seizure (periictal) 1. Prodromal psychiatric symptoms (prodromal mood or behavioural change). the mood

change is usually depressive or irritable, and may last from a few minutes to a few days.

2. Ictal psychiatric symptoms (e.g. ictal psychosis due to nonconvulsive status; ictal perceptual and affective changes, ictal automatisms)

3. Postictal psychiatric symptoms (e.g. postictal depression/psychosis). Post-ictal

confusional states are extremely common and often unrecognized; it may take from a few minutes to a few days to fully regain awareness, although the patient may superficially appear to have recovered.

B. Not temporally related to seizures (interictal) but with a presumed relationship

to the persons epilepsy syndrome (e.g. schizophrenia-like psychosis of epilepsy).

A. B. C. Related to the treatment of the persons epilepsy 1. Direct effects (e.g. vigabatrin-related psychosis) 2. Indirect effects (e.g., folate deficiency related to anticonvulsants causing depression;

gingival hyperplasia from phenytoin causing stigma and depression in an adolescent)

D. Related to psychosocial factors (e.g. self-esteem issues; stigma;

unemployment)

Two types of mood or affect change are found: (1) periictal, which are related to the ictus (or seizure), and (2) interictal, in which the disturbances are chronic and not directly related to the ictal discharge. Another sequelae of epilepsy, which interests psychiatrists is the schizophrenia-like psychosis which develops after many years of (usually) temporal lobe epilepsy. The link between psychosis and temporal lobe epilepsy is strong not only clinically

6

but also theoretically, because there is an acknowledged link between the limbic system and the modulation of emotional and social behaviours.

Risk Factors Associated with Interictal Psychoses of Epilepsy Sex Bias to females

Age of onset of epilepsy Early adolescence

Interval Onset of seizures to onset of psychosis: 14 years (average)

Epileptic syndrome Temporal lobe epilepsy

Seizure type Complex partial; automatism

Seizure frequency Low, diminished

Neurological findings Left-handed; abnormal neurologic examination

Pathology Gangliogliomas, harmatomas

EEG Mediobasal focus, especially left-sided

Head Injuries

Mental impairments (exacerbation of preexisting character, personality changes, chronic affective disturbance, intellectual deterioration, memory impairment, impaired concentration, dysphasia, psychotic changes) have all been described in patients with head injuries. Mental and physical impairments often coexist, compounding the total disability. As a general rule, if the duration of post-traumatic amnesia (also called anterograde amnesia and defined as the time from the moment of injury to the time of resumption of normal continuous memory) is greater than 24 hours, lasting cognitive impairment is likely. During the period of clouding of consciousness isolated islands of memory may occur; these are false end points for anterograde amnesia. The period to be measured is from the time of injury until continuous memory is restored.

Postconcussional syndrome is more commonly suspected and diagnosed after mild

injuries and when there are no clear pathological findings on diagnostic testing. Though neurological examination is usually normal in patients with this syndrome after minor injuries, deficits may often be demonstrated with neuropsychological testing.

7

Commonly Reported Symptoms of Postconcussional Syndrome Headache Insomnia Dizziness Hypochondriachal concern Fatigue Hypersensitivity to noise Diminished concentration Photophobia Memory problems Depression Irritability Diminished libido Anxiety Cerebrovascular Accidents

As with brain injury, cerebrovascular accidents are common and result in significant

psychosocial disability. The types of clinical disorders produced by vascular brain injury fall into two categories. One category includes disorders in which the brain injury is viewed as a cause of emotional disorders which are seen in patients without brain injury, e.g., depression, mania, anxiety disorders, and personality disorders. Stroke is strongly associated with depression and there is some evidence to suggest left hemisphere stroke is more strongly associated with depression than right hemisphere stroke, although this has not been replicated. The other category of emotional disorders that occur after brain injury includes those that are unique to brain injury, including catastrophic reaction (a sudden explosive outburst of rage and distress often prompted by the recognition of failing powers this may be the first signal of early organic impairment), the indifference reaction, anosognosia or denial of illness, aprosodia (the inability to comprehend or express emotion), and the pathological display of emotion. The causes of these disorders are also viewed from two perspectives, one a direct result of pathophysiological changes produced by brain injury or, alternatively, as empathically understood response to impairment and/or loss. Parkinsons Disease

Psychiatric manifestations of Parkinsons disease may be the consequence of

treatment or of the disease itself. These include bradyphrenia, an increased risk of depressive illness and an increased incidence of dementia. Depression is a common manifestation of Parkinsons disease occurring in about a third of patients in the community and about half of hospital patients. Psychosis occurs in 20-30% of patients and is frequently caused by treatment of Parkinsons disease and its therapy should, in the first instance, be directed at reducing or stopping the most recently added antiparkinsonian agent. Anticholinergics (benzhexol), L-dopa and amantidine all have a tendency to induce an acute organic reaction with vivid visual hallucinations. Many of the patients with mild cognitive decline exhibit the characteristics of subcortical dementia. Encephalitis

Symptoms and signs of encephalitis include fever, headache, confusion, dizziness,

vomiting, seizure and coma. Clinical signs of Nipah virus infection are similar to those of other viral encephalitis and need to be considered in any patient with encephalitis who has direct contact with live pigs. Cases of encephalitis have been described in which there is

8

minimal disturbance of consciousness, and odd behavioural changes have been attributed to conversion or a functional psychosis. Herpes simplex can cause focal inflammation and damage in any area of the brain, especially the medial temporal area. Postencephalitic syndrome has been described and its features include memory and concentration problems, agnosia, hyperorality, agitation and altered sexual behaviour. Brain Tumours

Primary tumours of the brain and meninges are common. Metastases from

carcinoma of the bronchus, breast, gastrointestinal tract and elsewhere account for 20% of intracranial neoplasms. Seizures are the most common presenting sign of brain tumour. Neuropsychiatric manifestations of brain tumours depend on the size and location of the tumour, whether intracranial pressure is increased (which may lead to difficulty in concentration, impaired consciousness, drowsiness, apathy and emotional flatness) and its rate of growth. Slow- growing tumours often produce mental symptoms without neurological signs. Frontal lobe tumours may manifest as frontal lobe personality change and remain relatively silent neurologically. Temporal lobe tumours may present as personality change, early cognitive deficits and complex visual hallucinations. An association with schizophreniform psychosis has been described. Though the incidence of brain tumour among psychiatric patients may be relatively low (less than 5% on autopsy), a significant percentage of these would have been treatable with early diagnosis. Dementia (see chapter on Geriatric Psychiatry) II. Neuropsychiatric consequences of systemic disease Endocrine Diseases

The patient with hyperthyroidism may have restlessness, over-activity, over-

reactivity, depression and poor concentration. The differential diagnosis between thyrotoxicosis and anxiety disorder depends on a history of distinctive symptoms and on physical examination. Affective (especially manic) and schizophrenic psychosis has also been described. With modern treatment, delirium in thyroid crisis has become rare. Hypothyroidism may have the following manifestations: mental lethargy, fatigue, apathy, irritability, psychomotor slowing and poor memory. Hypothyroidism, occurring in 5% of patients who are taking lithium carbonate, can be successfully treated with thyroxine. Myxoedema patients who are given thyroxine may symptomatically get worse before they get better. The bodys readjustment precipitated by the thyroxine intake may exacerbate emotional and physical difficulties. The patient with Addisons disease (hypoadrenalism) may present with apathy, depression, fatigue, irritability, memory difficulties, delirium or dementia. Cushings disease (hyperadrenalism) may manifest as a depressive illness. The severity of the depression is not related closely to plasma cortisol concentrations, and premorbid personality and stressful life events appear to predispose to the development of the affective disorder. Hypopituitarism may present as acute organic reaction, as coma or as depression, apathy, lack of initiative and somnolence.

9

Electrolyte Imbalance The signs of hyponatremia include fatigue, lassitude, apathy, muscle cramps and

seizures. Water intoxication, a cause of hyponatremia, is sometimes encountered in patients with chronic mental illness. It is important to avoid use of carbamazepine in patients with a history of compulsive water drinking as the drug may also contribute to hyponatremia. Hypokalaemic muscle paralysis may be diagnosed as hysteria, especially in cases of familial periodic paralysis in which the hypokalaemia may be triggered by emotional stress. Potassium depletion results is lethargy, apathy, anorexia, constipation, anxiety and depression. Renal Disease

Uraemia, particularly with a urea level above 40 mmol, causes an acute organic

reaction in one-third of cases. Other symptoms of uraemia include fatigue, depression and somnolence. Chronic uraemic patients show less deep sleep, less rapid-eye-movement sleep, and many myoclonic jerks. Sleep is worse the night after a hemodialysis session, possibly because of direct effects of the hemodialysis but partly because of schedule shifts and other encumbrances of the method. Since depression often occurs in response to loss and given that dialysis patients experience many losses (e.g., loss of strength, energy, sexual ability, work ability, physical freedom and life expectancy), it is not surprising that depression is frequent. Systemic Lupus Erythematosus (SLE)

The CNS is affected in 50-75% of lupus patients. Neuropsychiatric involvement is

attributed to the manufacture of anti-brain antibodies, which cause a breakdown in blood-brain barrier and the development of an allergic, autoimmune encephalitis. Seizures, disturbances of mental function and consciousness level, and cranial nerve palsies are some of the manifestations of cerebral lupus. Schizophrenic or affective psychosis and neurotic reactions have also been reported in cases with SLE. The most common autopsy findings in the brains of patients with cerebral lupus are microscopic infarcts and hemorrhages. Apart from direct involvement of the CNS, other issues worthy of consideration are the psychological sequelae of the patients awareness of the illness or its impact, and the psychiatric side effects of the drugs (e.g., steroids) used to treat the illness. HIV and AIDS Case History

A middle-aged Chinese man was arrested by the police who found him wandering in the streets stark naked and directing traffic. Mental state examination showed that he was elated and had grandiose delusions. Physical examination showed that he had extensive fungal infections of the oral cavity, indicating that he could be immuno-compromised. After the institution of neuroleptics his mood and cognitions improved and consequently, he was able to receive pre-test counselling and give informed consent for HIV testing. He was found to be positive for HIV and a diagnosis of organic mood disorder (mania) was made.

10

Psychiatric and behavioural problems associated with HIV infection might develop as psychological reactions or they may reflect underlying organic pathology. By its invasion of the CNS, HIV can cause a range of organic mental disorders. If an organic brain syndrome is suspected consider the following conditions: Primary HIV-related brain disorder

Secondary HIV-related brain disorder

Acute and sub-acute syndromes (delirium)

Dementia and minor cognitive disorder

Toxoplasmosis, progressive multifocal leucoencephalopathy, tumor (e.g. lymphoma)

Systemic disorder Secondary infections

Organic causes include direct infection of the brain, secondary process in the brain, complications resulting from the individuals immuosuppression and side effects of anti-retroviral medication. The most severe form of neurocognitive disorder is HIV-Associated Dementia, characterised initially by disturbances in learning new information, attention, and speeded information processing. Hallmarks include psychomotor slowing, and neuromotor signs such as ataxia and incoordination. A severe dementing syndrome characterised by amnesia, agitation, disorientation, mood and behavioural dyscontrol, extreme psychomotor slowing, and naming difficulties can occur as the dementia progresses. Inappropriate behaviour, labile affect, or aggression may also occur. Ultimately, the demented person becomes bedridden and may suffer from severe lack of coordination, weakness, and loss of bladder and bowel control. General Principles in Management 1. A thorough history, physical examination, mental state examination (including cognitive assessment) is essential. The following should alert one to perform a thorough physical examination: positive medication history or history of medical illness; abnormal vital signs on repeated assessment; presence of mental status changes suggestive of organic mental disorder (factors consistently related to organic pathology include visual hallucinations and old age); elderly patients showing new onset of mental status changes or qualitative change in existing mental status. 2. Evidence of impairment of intellectual or memory indicates the need for radiological investigation CT or MRI and examination of CSF. In HIV patients, one needs to look for treatable conditions such as opportunistic infections or lymphomas. 3. Neuropsychological evaluation would be useful in assessing patients level of intelligence, memory and other cognitive functions. Experience with the Weschler Adult Intelligence Scale suggests that verbal abilities are more resistant to impairment than performance and that a discrepancy of greater than 20 points between the two scales is a statistically significant indication of organic impairment. Apart from establishing the patients baseline, neuropsychological testing is useful in identifying patients strengths and deficits, which are important considerations when devising rehabilitation programs.

11

4. With regard to treatment of delirium, one needs to ensure sleep, maintain fluid and nutritional intake, and provide supportive nursing care. General measures include nursing in a quiet, well-lit room, with a clock and calendar to help maintain orientation, and asking nursing staff to communicate frequently with the patient. The restless, agitated, fearful patient should be mildly sedated with haloperidol. 5. The management of the psychiatric syndromes associated with various neurological and systemic illness is essentially similar to the management of these disorders in other contexts. However, special attention has to be paid to the increased risk of suicide. 6. Caution needs to be exercised when prescribing psychotropics. First, neurological patients may have increased propensity to develop extrapyramidal side effects. In HIV and AIDS patients, the use of atypical antipsychotic drugs such as olanzapine is less likely to cause extrapyramidal side effects than major tranquillizers such as haloperidol. Second, the possibility of drug interactions has to be borne in mind. In Parkinsons disease, for instance, there is interaction between fluoxetine and selegiline resulting in a confusional state. Third, in epileptic sufferers and head-injured patients, lowering of seizure threshold by psychotropics may exacerbate seizures and lead to postictal psychosis. It is also important to avoid using phenothiazines in delirium tremens because they are epileptogenic and the condition already carries a risk of seizures. Fourth, patients with renal or liver disease may have problems metabolising certain psychotropics, and caution needs to be exercised when choosing medications. 7. Close liaison with the medical specialists is of paramount importance, especially so when one needs to unravel the cause of the psychiatric morbidity. Prolonged high-dose steroids are a possible cause of psychiatric disorders in systemic lupus and renal transplant. Mania, a rare occurrence in Parkinsons disease, is usually due to dopaminergic treatment when present. 8. Psychosocial support for patient and his/her carers must also be provided. In addition to identifying and treating the underlying cause, the clinician needs to communicate effectively with the patient and his/her caregivers with regard to prognosis and other aspects of management. For patients with cognitive deficits, convalescent care and rehabilitation need to be planned. It is equally important to support other family members; regular family meetings may be required for such a purpose. Linkages with the relevant community support groups may need to be established, e.g. with Singapore Epilepsy Foundation (for patients with epilepsy), Singapore National Stroke Association (for survivors of stroke), Action for Aids (for HIV and AIDS patients), etc. References 1. William Alwyn Lishman, Organic psychiatry: the psychological consequences of

cerebral disorder (Third edition). Oxford, UK: Blackwell, 1998. 2. Kenneth H. Nott and Kavita Vedhara (ed). Psychosocial and biomedical interactions

in HIV infection. Amsterdam, The Netherlands: Harwood Academic Publishers, 2000. 3. Jeffrey L. Cummings, Michael R. Trimble. Concise guide to neuropsychiatry and behavioural neurology. Washington: American Psychiatric Press, 1995.

12

24 ORGANIC PSYCHIATRYNg Beng YeongTable 2. Patterns of Focal Loss

DeliriumCommon Causes of DeliriumC. Related to the treatment of the persons epilepsyRisk Factors Associated with Interictal Psychoses of Epileps

Early adolescenceCerebrovascular Accidents

II. Neuropsychiatric consequences of systemic diseaseCase History