Organic Mental Disorder

Organic Mental Disorders(1)

Department of psychology The first affiliated hospital of ZZU Huirong guo

Contents Preface Symptoms and signs of organic mental disorders action and behavior Etiology Factors affecting symptoms and signs

Preface  Organic mental disorders encompassed psychological and behavioral disorders whose abnormalities resulted from known biological causes and pathophysiological mechanisms( 病理生理机制 )  In contrast to these organic disorders, psychiatric illnesses such as schizophrenia or bipolar disorder were categorized as ”functional disorders” with no identifiable organic etiology

Preface 

Because this organic/functional dichotomy became increasingly problematic as evidence grew for central nervous system dysfunction in the major “functional” mental disorders  In addition, this dichotomy left clinicians with no satisfactory alternative term for conditions that were not “organic mental disorders.”

Preface  Finally, the organic versus nonorganic distinction encouraged the continued stigmatization of mentally ill individuals by suggesting that “functional” disorders such as schizophrenia were not true medical disorders

Preface 

So, in many articles, the disorders of delirium, dementia, and amnesia are classified as cognitive disorders( 认知障碍 ), other diagnoses previously classified within the organic mental disorder section are now called secondary if caused by a specific medical disorder or substance induced if substance intoxication or withdrawal is judged to be etiologically related to the disturbance

Symptoms and signs of organic mental disorders In evaluating a patient with a psychological or behavioral disturbance, certain signs and symptoms suggest that the disorder is a cognitive disorder, as described in this chapter. These signs and symptoms include the following

Symptoms and signs of organic mental disorders 1. 2. 3. 4. 5.

Fluctuating performance on serial mental status, examinations Memory impairment Disorientation Cognitive impairment, e.g. dyscalculia or reduced fund of information Visual hallucinations or illusions

Symptoms and signs of organic mental disorders 6.

Tactile hallucinations or illusions

7.

Motor restlessness （坐立不安） Impaired judgment and poor impulse control Autonomic symptoms Sudden onset without any previous personal or family psychiatric history—at any age, but particularly in a patient over 40

8. 9. 10.

Symptoms and signs of organic mental disorders 11. 12. 13.

Lack of expected response to traditional treatment Prior physical illness or current physical symptoms History of recent drug or medication intake

Symptoms and signs of organic mental disorders  Although any of these symptoms and signs may be present in any psychiatric disorder, when they are elicited, it is important first to consider cognitive disorders or secondary or substance— induced disorders in the differential diagnosis.

Etiology A single psychiatric syndrome may have many organic causes, and a single cause can result in different syndromes. For example, neurosyphilis （神经梅毒） can cause delirium, dementia, secondary psychotic disorder, secondary mood disorder, or secondary personality change and so on

Etiology Even in the same patient, a given cause may lead first to one syndrome and then to another. For example, neurosyphilis may first present as a secondary mood disorder or a secondary personality change, but then may progress to dementia  Similarly, infection with the HIV(human immunodeficiency virus)may cause a variety of disorders, including delirium, dementia, secondary psychotic disorder, and secondary mood disorder 

Factors affecting symptoms and signs 

Physical factors affecting symptoms and signs include the following :



The degree of insult sustained by the central nervous system (CNS) The rate at which whole—brain involvement occurs The physical condition of the patient

 

Factors affecting symptoms and signs     

Psychological factors affecting symptoms and signs include the following: The patient’ personality and psychological defense mechanisms The patient’s intelligence and education The patient’s level of prenorbid psychological adjustment The patient’s level of current psychological stress and conflict

Factors affecting symptoms and signs    

Social factors affecting symptoms and signs include the following: The degree of social isolation versus support The degree of familiarity patients have with their environment. The level of sensory input

Dementia  Definition

Dementia is a syndrome manifested by several cognitive deficits that include memory impairment involving at least one of the following: aphasia （失语） , agnosia （失认） , apraxia （失用） , or a disturbance in executive functioning （执行功能） that interferes with social, occupational, interpersonal skills

Dementia The most commonly used brief test for cognitive function is the Folstien Mini-Mental Status Examination (MMSE).

Characters of dementia The patient with dementia is forgetful, has difficulty learning new information, and will often try to minimize or deny deficits. Typically, recent memory is worse than remote memory. A patient may be unable to recall names of three objects after 5 minutes, but may have excellent recall of events that occurred in childhood.

Etiology and pathogenesis The pathogenesis of dementia depends largely on the etiology. Approximately 5-15%of all dementias are reversible, and if their cause is identified and treated the prognosis is good. On the other hand, neurodegenerative （神经 变性） dementias such as AD are progressive and incurable and ultimately end in death

Etiology and pathogenesis 1. 2. 3. 4. 5. 6. 7. 8.

Dementia of the Alzheimer’s type Vascular dementia Alcohol—related dementia Dementia due to Parkinson’s Disease Dementia due to Lewy Body Disease Frontal Lobe Dementia Other progressive Dementing Diseases Dementia due to Other Cause

Diagnosis In diagnosing a dementia the clinician must first aggressively rule out any potential reversible causes of the disorder. Ideally, a complete history should be obtained form someone who knows the patient well, as well as from the patient  Attentions should be paid to medications, drug and alcohol use, onset and course of impairment, as well as psychosocial and medical antecedents. 

Diagnosis A

physical examination should be performed with full neurological evaluation.  A comprehensive mental status examination should be performed, as should a standardized cognitive measure such as the MMSE

Criteria Symptoms criteria: When there is evidence of organic mental disorders General impairment of intelligence Cerebral atrophy shown in CT or MRI  Severity criteria: The condition has resulted in impairment in activities of daily living and social functioning  Course criteria: The disease takes an insidious, progressive and irreversible course. It is not uncommon that the progression of disease becomes arrested at some stage of illness 

Differential diagnosis 

Distinguishing dementia from other cognitive disorders and from both primary and secondary psychiatric disorders is critical  Common clinical dilemmas in geriatric care are distinguishing dementia from depression, delirium, or the cognitive change of normal aging.

Differential diagnosis Chronically mentally ill patients may also be incorrectly diagnosed with dementia  There is also debate whether chronic schizophrenia can be a primary etiology of dementia  A chronic schizophrenic patient with profound social regression and severe negative symptoms may be difficult to distinguish from a patient with dementia 

Treatment 

Psychosocial treatment of dementia There is a wide range of psychosocial strategies used to improve the quality of life and maximize function. These can be classed as cognitive, behavioral, environmental, integration of self （自身整合） , and socialization （社会活动） and memory.

Treatment  Pharmacological  

treatment of dementia

Pharmacological treatment for slowing the rate of cognitive decline Pharmacological treatment for related psychiatric conditions

Delirium

Delirium  Definition: 



Delirium is a transient, potentially reversible dysfunction in cerebral metabolism, etiologically related to metabolic derangements, that has an acute or subacute onset and is typically manifested by alterations of levels of consciousness and change in cognition It is the most common psychiatric syndrome found in a general medical hospital, particularly among older patients

Definition  The

delirium syndrome may manifest itself in numerous ways, but key to the presentation is a change in the level of consciousness, from a hyperactive increased arousal and psychomotor activity, a hypoactive decreased arousal and psychomotor activity, or a mixed form with fluctuations between states

Definition The diagnostic features of delirium in DSM-Ⅳ : 



1 、 Disturbance of consciousness (i.e. reduced clarity of awareness of the environment), with reduced ability to focus, sustain, or shift attention. 2 、 Change in cognition (such as memory deficit, disorientation, language disturbance) or the development of a perceptual disturbance that is not better accounted for by a perrxisting or evolving dementia.

Definition 3、

The disturbance that develops over a short period of time (usually hours to days) and tends to fluctuate during the course of the day.  4 、 Evidence from the history, physical examination, or laboratory findings of a general medical condition, substance intoxication or withdrawal and/or medication side effect judged to be etiological related to the disturbance.

Epidemiology  Past

research has been confounded in part by variability of diagnostic criteria  Current data indicate that delirium occurs in 10-20% of patients on acute medical/surgical wards  Some authors report that the incidence of delirium in elderly patients presenting to the emergency room is as high as 80%

Epidemiology  Delirium

is infrequent in the young and middle-aged and, when present, is often associated with alcohol or illicit drug use  The incidence of delirium increases progressively with each decade past the age of 40

Epidemiology 

Risk factors for developing delirium :

(1)

elderly patients, patients with preexisting brain damage (e.g. dementia, strokes), patients on polypharmacy or withdrawing from addictive substance, medically compromised patients (e.g. individuals with AIDS, burn patients)

(2) (3) (4)

Etiology & Pathogenesis  Advanced

age is one of the most important risk factors for developing delirium

Etiology & Pathogenesis  The

physiological basis of delirium is poorly understood

Failure of cerebral oxidative metabolism with a subsequent decrease in neurotransmitter production  Cholinergic （胆碱能） dysfunction as an etiology of delirium  Lymphokines （淋巴因子） have been shown to influence delirium in individuals with inflammation and infection 

Etiology & Pathogenesis  The      

potential cause of delirium

Infections Withdrawal Acute Metabolic Trauma CNS Pathology Hypoxia （低氧）

 Deficiencies

 The

potential cause of delirium

Endocrinopathies （内分泌病）  Acute Vascular:  Toxins or Drugs 



Heavy Metals

Diagnosis As many as 19 of 20 delirious patients are not accurately diagnosed  A detailed history should always be obtained, when possible from collateral and recent cognitive and behavioral changes  A full medical and psychiatric history should also be obtained  Attention should be given to recent trauma, exposure to infections, medication use, including over-the-counter drugs, and alcohol and illicit drug use

Diagnosis Mental status testing is essential  the

Folstein Mini-mental Status Examination (MMSE)  the Delirium Rating Scale  physical examination should include vital signs, cardiac and respiratory status, and upper motor neuron and other focal neurological functioning

Differential Diagnosis Delirium Onset

Dementia

Rapid

Slow and progressive

Reversibility Potentially reversible

Usually not reversible

Deficits

Focal cognitive

Global cognitive

Affects attention primarily

Affects memory primarily in early stages

Fluctuating level of aware ness

Level of awareness intact in early stages

Fluctuating level of attention

Level of attention usually intact in early stages

Course

Urgency

Fluctuating and variable over course of day Needs immediate workup

Typically no fluctuations

medical Nonurgent

acute

usually

daytime

Treatment The treatment involves :  treating the primary causative condition  providing supportive care  and preventing injurious behaviors

Treatment  General

principles of managing delirium are used for all patients. These include providing fluids and nutrition, providing a calm quiet environment, and establishing appropriate sleep cycles  The patient needs to be frequently reoriented and explanations should be given for almost all activity involving the patient

Treatment  Either

physical or pharmacological restraints may be necessary when behavioral and supportive measures are ineffective  Pharmacological intervention is sometimes necessary

Prognosis 



Delirium carries a high risk of morbidity and mortality, long-term institutional placement, and cognitive decline. Many cases of subclinical dementia are unmasked by delirium. Consequences of the immobility and confusion associated with delirium include dehydration, malnutrition, and decubiti. Among delirious hospitalized medical patients mortality is as high as 20-40%

Prognosis Many delirious patients recover their premorbid cognitive functioning completely when the delirium is reversed.  Those most likely to fully recover are patients with identifiable and completely treated medical conditions such as an infection and those with drug-induced delirium 

Illustrative case A 43-year-old woman

Amnestic disorders Definition

DSM-Ⅳ diagnosis criteria for amnestic disorder related to a general medical condition:

Definition 



A. The development of memory impairment as manifested by the inability to learn new information or the inability to recall previously learned information B. The memory disturbance causes significant impairment in social or occupational functioning and represents a significant decline from a previous level of functioning

Definition 



C. The memory disturbance does not occur exclusively during the course of delirium or dementia D. There is evidence from the history, physical examination, or laboratory findings of a general medical condition (including physical trauma) judged to be etiologically related to the memory impairment

Causes of amnestic disorder Korsakoff’s syndrome  Brain trauma  Cerebral anoxia  Cardiac arrest （心跳停止）  Acute respiratory failure  Anesthetic accident （麻醉意外）  Carbon monoxide poisoning （ CO 中毒）  Drowning  Strangulation （窒息） 

Causes of amnestic disorder Space-occupying lesions （占位性病变）  Neoplasms  Abscess  Subarachnoid hemorrhage （蛛网膜下腔出血）  Cerebrovascular accident  Infarction of posterior cerebral artery distribution  Bilateral hippocampal infarction 

Causes of amnestic disorder  Infection  

Herpes simplex virus encephalitis Tuberculous

 meningitisElectroconvusive

therapy(ECT)  Temporal lobe epilepsy

Causes of amnestic disorder  Transient

global amnesia  Acute hypoglycemia （低血糖）  Substance induced  

Anticholinergic agents Benzodiazepines



Heavy mental poisoning

Epidemiology  Amnesic

disorder is relatively uncommon. No adequate studies exist on the incidence or prevalence of amnestic disorders  Amnesia is most commonly found in alcohol use disorders and in the head injury

Epidemiology  Recent

trends suggest a decrease in the frequency of amnesia related to chronic alcohol use and an increase in the frequency of amnesia secondary to head trauma

Etiology & pathogenesis  The

major neuroanatomical structures involved in memory and in the development of amnestic disorders are diencephalic （间脑） structures such as the thalamus （丘脑） (dorsomedial and midline nuclei 中线核 ) and medical temporal lobe structures, such as the hippocampus （海马） , mamillary bodies, 纹 状体 and amygdala 杏仁核

Etiology & pathogenesis  Among

alcoholics, the most common cause of amnestic disorder is thiamine deficiency  Other causes of amnestic syndromes include head trauma, cerebrovascular disease, multiple sclerosis, hypoxia, hypoglycemia, herpes simplex encephalitis, space-occupying lesions, medications, seizures, and electroconvulsive therapy

Etiology & pathogenesis  Transient

global amnesia is a variant of amnestic disorder. It is characterized by the acute onset of retrograde and antegrade amnesia, which typically resolves within 6-24 hours

Diagnosis  Must

have impairment in memory and new learning with otherwise preserved intellectual functioning  Memory loss is antegrade or retrograde  The onset of symptoms may be sudden, as in head trauma, or gradual, as in thiamine deficiency

Diagnosis  The

course and prognosis of an amnestic disorder are variable and contingent on the specific cause  Transient amnestic disorder with full recovery can be seen in electroconvulsive therapy, benzodiazepine use, and epilepsy

Differential diagnosis  normal

aging memory impairment  With dementia, memory loss occurs alongside other cognitive deficits  In delirium, memory loss is accompanied by impairment in attention and concentration  Other disorders that may resemble an amnestic disorder include the dissociative disorders, factitious disorder, and malingering

Treatment  Treatment

of amnestic disorder must begin, whenever possible, with identifying and treating the underlying cause, for instance, giving thiamine to an individual with chrinic alcohol use who is at risk for Wernicke’s encephalopathy and Korsakoff’s syndrome  Typically, in such a case, 100mg of thiamine per day is given intramuscularly for the first 3 days, followed by 100mg of thiamine per day given orally until nutritional status improves

Treatment  Otherwise,

treatment is typically supportive, including psychodynamic and cognitive-behavioral therapy, and educating patients and their families

Illustrative case A 28-year-old married construction worker who was transferred to the psychiatric hospital from a medical ward

Summary 1. It is often difficult by clinical presentation to determine whether psychiatric symptoms are caused by dementia, delirium, amnesia, or other cognitive disorder, are secondary to a general medical condition or are substance induced, or are part of a primary psychiatric disorder. Symptoms and signs that point toward a diagnosis of a cognitive or secondary psychiatric disorder are reviewed at the beginning of this chapter.

Summary 2. A vigorous search for an underlying cause for the presenting psychiatric symptoms is important in any case in which a diagnosis other than a primary psychiatric disorder is suspected. If a specific cause is identified and is treatable, some or all of the psychiatric symptoms may be reversible

Summary 3. In addition to identifying and treating any underlying cause, important aspects of treatment include supportive care, education of patients and their families, and the judicious use of psychoactive medications to control psychiatric symptoms

Organic Mental Disorders(2)

Contents Disease （老年性痴呆）  Vascular Dementia （血管性痴呆）  Epilepsy ( 癫痫 )  Head Injury （头部外伤）  Intra-cranial Infections  Deterioration diseases （变性性疾病）  Metabolic and Endocrine Disorders  Alzheimer’s

Alzheimer’s Disease

Alzheimer’s Disease Alzheimer’s disease results in an insidious, progressive dementia with no specific identifiable cause, and no abnormal peripheral laboratory  It is a diagnosis of exclusion made after ruling out other cause of dementia. The clinical features and pathology of this condition were first fully described in 1906 by Alzheimer in a cause report of a 51 old woman. 

Prevalence  The

investigation in USA indicates that between 2% and 4% of the population over age 65 years is estimated to have dementia of Alzheimer’s Type. The prevalence increase with increasing age, particularly after age 75 years

Etiology & Pathogenesis  The

electroencephalogram often should diffuse slowing  Brain imaging with either CT or an MRI scan will often reveal cerebral cortical atrophy and slight to moderate ventricular dilatation

Etiology & Pathogenesis  Functional

brains scans (PET or SPECT) may show decreased metabolism primarily in the temporoparietal areas bilaterally  Histopathological changes in dementia of Alzheimer’s type include microscopic senile plaques (composed primarily of amyloid), neurofibrillary tangles, etc.

Etiology & Pathogenesis  Other

findings include profound loss of large cholinergic neurons in nucleus basalis, decreased amounts of choline acetyltransferase(CAT), the enzyme involved in the synthesis of acetylcholine in the cerebrospinal fluid.  Dementia of Alzheimer’s type also results in the loss of noradrenergic neurons in the locus ceruleus and serotonergic neurons in the dorsal raphe nuclei.

Etiology & Pathogenesis  Peptide

neurotransmitters are also affected. (Decreased levels of somatostain, substance p, corticotropin-releasing factor, and gaminobutyric acid )  Dementia of Alzheimer’s type probably has a multifactorial etiology in which genetic and environmental factors combine with aging to overcome the ability of neurons to maintain homeostasis.

Etiology & Pathogenesis  This

impaired neuronal metabolism results in damaged mitochondria, damaged cytoskeleton, increased release of the excitotoxic neurotransmitter glutamate, aberrant phosphorylation of membrane proteins, and, ultimately, premature dysfunction and death of neurons

Signs & Symptoms  The

onset is insidious and occurs from middle age onwards  The course is progressive with death occurring usually in 3-7 years.

Signs & Symptoms  In the early stages, failing memory, perplexity, and mood disturbance (usually agitation) are most obvious  After a year or so, there is more rapid deterioration followed by parietal and extrapyramidal symptoms and eventually by ‘primitive’ reflexes (sucking, glabella tap, tonic grasp) and generalized bodily wasting

Treatment  Enhancing

the cholinergic system may be therapeutic. However, attempts to treat these patients with acetylcholine precursors such as choline and lecithin or with direct cholinergic agonists such as arecoline, bethanecol, or pilocarpine have not been successful  Enhancing the cholinergic system by inhibiting acetylcholinesterase does, however, show some promise

Treatment  Studies

with tetrahydroaminoacridine (also known as THA or tacrine) have inconsistently found positive results, but the drug cause hepatotoxicity in some patients; however, it was recently approved for use in the United States  Hydergine is an ergoloid mesylate also approved in the United States for the treatment of dementia of the Alzheimer’s type; however, its mechanism of action is unknown

Treatment  Other

type of agents under investigation include calcium channel blockers (nimodipine), angiotensin-converting enzyme inhibitors (captopril), selective monoamine oxidase type B inhibitors (selegiline), and nootropics-agents that (through an unknown mechanism of action) enhance neuronal metabolic activity (oxiracetam, acetylcarnitine, idebenone)

Treatment  Studies

of drugs to treat dementia are difficult because of peripheral metabolism of the drug, poor penetration of the blood-brain barrier, erratic absorption, and systemic adverse effects  In addition, since dementia of the Alzheimer’s type results in derangement of many neurotransmitter systems, treatment approaches targeting a single system appear less successful than combined treatment approaches

Treatment A

supportive treatment and careful nursing are also very important, which were discussed in the chapter of “Dementia”

Vascular Dementia

Vascular Dementia Although vascular dementia has several types, muti-infarct dementia (MID) is reported much more common and will be mainly discussed

Prevalence  Vascular

dementia accounts for 10-20% of dementia diagnosed in the patients over 65 years of age. MID is much less common than dementia of Alzheimer’s type

Etiology  Thromboembolic

cerebrovascular disease causes multiple infarctions of brain tissue  Typically, patients have a history of hypertention and possibly of strokes. Large and small cortical and subcortical inischemic changed result in decreased volume of brain tissue and the functional disconnection of the cortex

Etiology  Brain

imaging in these patients usually reveals evidence of the multiple infarctions, often coupled with diffuse white matter changes  Functional imaging with a PET or SPECT scan will usually show a patchy reduction in cerebral blood flow

Clinical features & Diagnosis  Patients

are characterized with cognitive deficits with focal neurological signs and symptoms, have an abrupt onset with a stepwise deteriorating course, and demonstrate a patchy distribution of deficits, depending on the location of the infarcts

Treatment  Patients

with vascular dementia may have some improvement in their cognitive functioning if they abstain from smoking and are treated judiciously for their hypertension. Aspirin, 325 mg each day, may improve the cognitive functioning of patients with vascular dementia, and hydergine has also been studied; however, the results have been inconsistent  Treatment for these patients is aimed primarily at preventing recurrent ischemic episodes

Epilepsy  History  



Epilepsy has long been held to be associated with mental disorder In the nineteenth century, it was though that personality deterioration and dementia were inevitable in epileptic patients a belief that continued well into the present century It is now known that most people with epilepsy can lead full and almost normal lives, and over two-third of them are free psychiatric problems

Etiology & Pathogenesis  Intellectual

impairment  Personality problems, especially if extensive brain damage  Epilepsy is common in the mentally retarded

Clinical features  Increasing

tension, irritability, and depression are sometimes apparent for several days before a seizure  Transient confusional states and automatisms may occur during seizures  Less commonly, non-convulsive seizures may continue for days or even weeks

Clinical features  Personality

deterioration (epileptic personality )



The social limitations imposed on the epileptic, his own embarrassment, and the reactions of other people



Brain damage

Clinical features  Psychological 

There was no evidence that these neuroses had a distinctive pattern

 Psychotic 

problems

disorder

Most recent research has concentrated on possible association between certain forms of epilepsy and schizophrenia-like disorders

Clinical features  Affective 



disorder

The relationship of epilepsy to affective disorder has been studied less thoroughly than its relationship to schizophrenia Some writers pointed out that postical confusinal states were sometimes misdiagnosed as affective disorders and further studies should be carried out

Diagnosis  The

clinical diagnosis depends upon detailed accounts of the attacks given by witnesses as well as by the patient  The history  The physical examination  Special investigations are concerned with etiology (initial findings, the type of attack, and the patient’s age )  EEG

Treatment  Antiepileptic 



The choice of drug is based more on freedom from adverse effects than on any difference in effectiveness in controlling seizures For partial (otherwise called focal) seizures, whether complex or simple in type

 carbamazepine 

drugs (anticonvulsants )

phenytoin

Treatment 

For tonic-clonic generalized seizures



The first choice lies between carbamazepine and sodium valproate



For absence seizures



sodium valproate is the first choice with ethosuximide as the alternative

 

For the status epilepticus Diazepam, given intravenously

Head Injury  Two

main kinds of patients who have suffered a head injury

First there is a small number of patients with serious and lasting psychological sequelae, such as persistent defect of memory  Second there is a larger group with emotional symptoms and anergia; symptoms are less obvious and may be easily overlooked, but they often cause persistent disability 

Acute psychological effects  Impairment

of consciousness  Memory disorders  Acute post-traumatic psychosis

Chronic psychological effects  Lasting

cognitive impairment  Personality change  Neurosis  Schizophrenia-like syndromes

Treatment  Planning

begins with a careful assessment of three aspects of the problem.

  

The first is the degree of physical disability. Second any neuropsychiatric problems should be assessed and their future course anticipated Third, a social assessment should be made

Treatment  physical

rehabilitation  Psychiatrical & psychological therapy  Practical and social support  Any problems of compensation and litigation

Intra-cranial Infections  Encephalitis  General

paresis  Creutzfeld-jacob Disease

Encephalitis A

primary viral disease of the brain or a complication of bacterial meningitis, septicaemia, or a brain abscess

 sometimes occurs after influenza, measles,

rubella, and other infectious diseases, and also after vaccination

Clinical features  In

the acute stage headache, vomiting, and impaired consciousness are usual, and seizures are common  An acute organic psychiatric syndrome  Predominant psychiatric symptoms  The complications that follow the acute episode; these may include prolonged anxiety and depression, dementia, personality change, or epilepsy  In childhood encephalitis may be followed by behavior disorders

General paresis  General

paresis is three times more common in men than women

 

usually starts between the ages of 30 and 50 The time from infection to symptoms is generally thought to be between 5 and 25 years

Clinical features  Minor

emotional symptoms or evidence of personality changes such as moodiness, irritability, or apathy, which precede evidence of intellectual impairment  About half the patients present more urgently, often with a striking lapse of social conduct such as indecent exposure, or sometimes with a seizure

Clinical features  Neurological

examination usually reveals abnormalities, most often Argyll Robertson pupils, tremor, and dysarthria  As the disease progresses there is increasing dementia, spastic paralysis, ataxia, and seizures  In untreated cases death usually occurs within four to five years

Creutzfeld-jacob Disease  This

uncommon disorder was described by Creutzfeld in 1920 and independently by Jacob in 1921  A rapidly progressive degenerative disease of the nervous system characterized by intellectual deterioration and various neurological deficits  The nature of the transmissible agent remains uncertain but it is often referred to as a ‘slow virus

Deterioration diseases  Multiple

sclerosis  Parkinson’s disease  Pick’s disease

Parkinson’s disease  Obvious

mental slowing  Memory difficulties , dementia is ‘subcortical’  The association of Parkinson’s disease as an appropriate response to the limitations of an unpleasant disease

Parkinson’s disease  The

drugs used to treat Parkinsonism may cause organic mental disorders

Anticholinergic drugs may cause excitement, agitation, delusions, and hallucinations  Levodopa is also associated with an acute organic syndrome and with depressive symptoms  Stereotactic surgery for the treatment of tremor often produces transient deficits in cognitive function 

Metabolic & Endocrine Disorders  Folic

acid deficiency  Hyperthyroidism  Hypothyroidism  Corticosteroid treatment

Folic acid deficiency  Among

the elderly and among psychiatric patients of all ages, it is common to find folic acid deficiency of dietary origin

 Low serum concentrations of foliate and low

red cell levels are usually common in epileptic patients  these deficiencies may account for some of the psychological symptoms of epileptic patients

Hyperthyroidism  Restlessness,

irritability, and distractability  The differential diagnosis between thyrotoxicosis and anxiety neurosis(a history of distinctive symptoms and physical examination )  Discriminating symptoms of thyrotoxicosis are

preference for cold weather and weight loss despite increased appetite

Hyperthyroidism  The

most discriminating signs of thyrotoxicosis are: a palpable thyroid, sleeping pulse above 90 beats per minute, atrial dibrillation, and tremor. T3 and T4 should be measured

 Mild

degrees of memory impairment

 Depressive

disorder, mania, or schizophrenia

Hypothyroidism  Lack

of thyroid hormones invariably produces mental effects  In early life, it leads to retardation of mental development  In adult life, it leads to mental slowness apathy, and complaints of memory

Hypothyroidism  Poor

appetite and constipation, generalized aches and paons, and sometimes angina  On psychiatric examination, actions and speech are found to be slow, and thinking may be slow and muddled  The features are non-specific (deep coarse voice; dry rough skin and lank hair; slow pulse, and delayed tendon reflexes )

Hypothyroidism A

slowly progressive dementia or more rarely there may be serious depression or schizophrenia  Paranoid features are said to be common in all the conditions 

Replacement therapy

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