Educationals

Parkinson's Disease and Depression

Parkinsonism is a relatively common neurological disease. Mild depression can be a prodromal feature in a small proportion cases. More commonly it occurs some time later in the course of the disease in 30 to 45% of cases. Like may other types of depression this is also common in females than in males. It is equally common in post-encephalitis, arteriosclerotic or idiopathic cases of Parkinson's disease.

An association between depression and Parkinson's disease is well established. Parkinsonian patients have a much higher incidence of depression that other patients of the same age who have physical disabilities. It is also more frequent in those patients who have accompanying dementia.

The depression can be reactive. It sets in as soon as the patient is informed about the nature of the disease, or later as a result of limitations due to the disability. This may lead to a reluctance to co-operate. About 25 to 50% of patients with Parkinsonism develop intellectual deterioration as the disease progresses. The severity of dementia correlates with the severity of Parkinsonian features especially the bradykinesia.

As opposed to bradykinesia, there is a bradyphrenia or subcortical dementia in Parkinsons disease. This is recognised by an undue delay in the production of appropriate verbal responses in a co-operative patient who has no communication difficulties. It is due to slowing of the mental processes and not of the motor processes. The psychological difficulties observed are changing
mental concepts, defective attention and motivation.

Psychological defects similar to bradyphrenia are also seen in depression. This relationship between affect or mood and speed of cognition is closely linked, and there may be a overlap between depression and Parkinsonism.

The mesocortico-limbic system may be impaired in both conditions. Reduced turnover of dopamine, serotonin and nonadrenaline has been reported in retarded depression.

In some cases, the degree of depression is disproportionate to the degree of disability. The depression may respond to anti-depressants or electroconvulsive treatment (ECT) while the disability may not.

Parkinsonian patients with depression exhibit hopelessness, pessimism, decreased motivation, increased pre-occupation with health and emotional liability. Impaired short term memory which is a feature of primary endogenous depression is absent. There is less self blame, guilt, worthlessness and self destructive feelings or behaviour compared to primary endogenous depression.

Treatment

The effect of l-dopa on mood is variable. Most patients experience an improvement in the mood. However, depression and suicide have also been reported, especially if the depression was present prior to starting l-dopa treatment. Antidepressants and electroconvulsive treatment effectively relieve the depressive symptoms and are not contraindicated. As a matter of fact, improvement in the Parkinsonian symptoms is seen sometimes during a course of ECT.

Changes in mood after stereotaxic surgery are also variable. Depression often improves after ventrolateral thalamic nuclei surgery. However, a high incidence of anxiety and depression in the first nine months after surgery has also been reported. The varying results may be explained by the premorbid psychiatric status of the patient, the precise site of the lesion and the effects of surgery.

Epilepsy and Depression

Epilepsy and depression are both common conditions and depression is a frequent complication of epilepsy. This has been observed since antiquity even as far back as in the time of Hyppocrates.

The depression can be related ictally or post ictally.

Ictal depression occurs with temporal lobe seizures, during status epilepticus, petit mal status and partial seizure status. Fears and depression are the commonest ictal experiences.

Interictal depressions are common in patients with late onset epilepsy, in children, and in complex partial seizures. There is a relationship between declining fits and emerging depression. The longer the duration of epilepsy the more severe the depression. There is no relationship between depression and the age of onset of epilepsy, or frequency of epilepsy. Depression is more closely related to temporal lobe epilepsy than to other types of epilepsy. The depression can last for months. Laterality of lesion responsible for depression reported is controversial as both dominant hemispheric as well as non-dominant hemispheric lesions have been involved.

60% of epileptic patients with depression have interictal dysthymia or reactive depression. Endogenous depression can also occur. It is more common than mania.

The neurotic or reactive depression is accompanied by fluctuating anxiety and dysphoria in the form of sporadic irrtability and aggressiveness.

The onset and subsidence of depression tends to be sudden and the mood disorder fluctuates markedly. Paranoid features frequently accompany the depression as well as depresonalisation, anxiety and hostility. There may be family history of depression in more than 50% of cases.

The suicidal rate is higher among epileptics than in the general population. The mortality is higher among mentally abnormal epileptics. Temporal lobe epileptics carry the greatest risk. Suicidal attempts are more common than successful suicides and multiple attempts are seen in 50% of cases, The ratio is twice as greater in men than in women. Most of them use their current
antiepileptic medication for suicidal purposes.

Patients receiving carbamazepine are the least depressed while patients receiving phenobarbitone are the most depressed. The level of psychopathology correlates positively with phenobarbitone and negatively with carbamazepine.

Low foliate levels in serum, RBCs and CSF have been demonstrated in epileptics with mental symptoms including depression. Folic acid supplements do not influence the onset of prognosis of the depressive state. However S-adenosylmethionine which is involved in folate metabolism seems to have antidepressant properties. The folic acid metabolism is least affected by carbamazepine and sodium valproate.

Treatment

Epileptic patients need a higher dose of antidepressants. All non-MAOI and some MAOI antidepressants lower the sedation threshold and can potentially aggravate clinical seizures. Therapeutic doses of antidepressants can do this in predisposed individuals who have a family history of epilepsy, existing brain damage or previous history of electroconvulsive therapy. patients receiving anticonvulsants demonstrate lower antidepressant level than patients who are not receiving anticonvulsants. Tricyclic antidepressants when given in high doses to patients receiving anticonvulsants may precipitate seizures, hence adjustment of dose of anticonvulsants may be required.

Electroconvulsive therapy is not contraindicated in epilepsy and can be life-saving in suicidal epileptics. Some epileptic patients may have a higher seizure threshold for ECT.

Reduction in polypharmacy may improve the medical state in some patients and so also can switching over to carbamazepine treatment.

In conclusion, the common psycho-social variables in epilepsy with depression are the chronicity of the disability, repeated unconsiousness leading to morbidity, uncertainty, loss of self esteem, social stigmatisation, difficulty in finding a job and loss of dignity. The implicated biochemical abnormalities are, disorders of noradrenaline, dopamine, serotonin, and gamma-aminobutyric acid metabolism and malfunctioning of the hypothalamic, pituitary axis and disturbances in folic acid metabolism.