In this review article, based on a literature study, present ideas upon the relation between M. Parkinson and concomittant depression are dicussed. After a short introduction, it is demonstrated that epidemiological studies show that a common pathophysiological basis can be assumed. Briefly pheno-menological aspects are mentioned, whereafter the changes in the different neurotransmittersystems are discussed in greater detail. The ratio of dopaminergic and serotonergic activities in the basal ganglia constitute an important determinant for the severity of motor symptoms in Parkinson's disease. Reduced serotonergic metabolism may be a compensatory mechanism for the reduced dopaminergic activity. At the same time, a reduced serotonergic activity can predispose to a depression. Lower activities in parts of the dopaminergic, serotonergic and noradrenergic systems may each be responsible for part of the affective symptomatology in depressed Parkinson patients.

Recently, some investigators have reported blunted natural killer cell activity (NKCA) in patients with major depression. In addition, there were some reports on negative relationships between NKCA and the occurence of negative life events. In order to replicate the above findings, the present study investigates NKCA and negative life events in 11 normal and 35 unipolar (minor, simple major, melancholic) depressed subjects. NKCA has been determined by all subjects. They completed the Questionnaire on Recently Experienced Events with scores on number and impact factor of events related to a) illness, b) working conditions, c) social relationships, d) housing problems, e) loss of possession. Depressed subjects reported higher scores on number and/or impact factor of events related to illness, social relationships and housing problems. In our investigation NKCA was significantly blunted in depressed subjects and, particularly in melancholies. So NKCA is negative correlated to the severity of depression. We were unable to detect any significant relationship between NKCA, and life events ( number of impact factors ), Our results do not corroborate the thesis that life events may affect immune function, as assessed by NKCA.

Systemic lupus erythematosus (SLE) is an autoimmune disease with a large variety of clinical signs. Delirium, affective disorders, psychoses, anxiety disorders, personality changes or combinations oftheforementioned are the mental disorders frequently encountered with SLE. There are only few indications for an obvious pathogenic mechanism responsible for the mental disorders occurring with SLE. It seems that the psychopathology in SLE largely is reactive in its nature and as such related to the presence of a serious disease. Psychotic features are possibly an exception because they may be related to pathological changes in the brain of the SLE patient. The administration of corticosteroids is not responsible for the psychiatric syndromes observed in SLE.

Research on the phenomenon of self-injurious behaviour (SIB) has been very limited despite the relative high prevalence of this type of disorder. The relative lack of knowledge of psychopathology in this field and the methodological problems in performing research projects may have contributed to the limitations in the interest for this area. Recently, research into biological aspects of the etiopathogenesis of SIB has yielded results that might open new vistas for a rational and effective pharmacotherapeutical approach. In this concise review the psychiatric, neurological, biological, pharmacological and methodological aspects of SIB in mental retardation will be mentioned.

The parasomnias are important yet badly recognised dysfunctions in clinical psychiatry. The clinical presentation and consequences in adults differ considerably from the often benign dysfunction in childhood. We present a case of incubus in a patient suffering from recurrent unipolar affective psychosis (type mania). The polysomnographic features are discussed and the differentiation from other paroxysmal amnestic conditions is emphasized. Pathophysiology encompasses a Slow Wave Sleep (SWS) arousal disorder probably related to a serotoninergic dysfunction. The relationship withpsychopa-thology is discussed.

Slowly progressive aphasia is an uncommon presenting symptom of a degenerative neurological disorder which in most cases eventually leads to a global dementia. The early recognition of this syndrome is sometimes hampered by the presence of accompanying or pre-existing psychiatric symptomatology. This is illustrated by two case reports. After a brief reflection on the nosological status of the disorder, the clinical picture and diagnosis are discussed.

In this paper a case history is described of a young male patient who gradually developed progressive personality changes and psychiatric complaints. This was subsequently followed by neurological symptoms and dementia. The patient appeared to be suffering from the adult form of metachromatic leucodystrophy (MLD). MLD is a rare disease with an autosomal-recessive mode of inheritance. The pathogenesis involves a deficiency of the enzyme arylsulfatase-A, causing sulfatide accumulation in (among others) nervous tissue.

Based upon a review of the literature several subtypes of MLD are mentioned. Both diagnostic aspects and therapeutic possibilities are critically discussed. It is argued that in cases of psychiatric complaints which do not easily fit in the diagnostic framework of the DSM-III-R in adolescence, the existence of neuropsychiatric diseases should be evaluated.