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A seventy year old right handed woman presented progressive limb apraxia and headache due to carbon monoxide poisoning. Thereafter, when in hospital for one week, she developed akinetic mutism, coma and died. Limb apraxia has been rather uncommonly reported in carbon monoxide poisoning. The akinetic mutism observed after the patient had been removed from intoxication could be analysed as a delayed encephalopathy related to a chronic carbon monoxide poisoning.

A 86 year old man suffered multiple palsies of the right V, VI, VII, VIII, IX and X cranial nerves preceded for several weeks by transient diplopia, facial palsy and vertigo. The CT scan and MRI showed two infarcts sitting in the territories of the right postero-inferior cerebellar artery and the right antero-inferior cerebellar artery. A cerebellar syndrome developed several days later. Although cranial nerves palsies are very commun following infarcts of the cerebellar arteries, their occurrence without other neurological deficit, especially cerebellar syndrome, seems to be rare.

A 65 years old woman with chronic high blood pressure and diabetes mellitus presented with a mutism akinetic of sudden onset and a right total hemiplegia with a Babinski sign secondary to a left anterior cerebral artery infarction. She had had six months earlier a transient gait disturbance. At that time, the CT scan showed lacunar infarcts of the head of both caudate nuclei. Neuropathological examination revealed that the left infarction of the anterior cerebral artery involved the superior frontal gyrus, the supplementary motor area, the cingulate gyrus and the corpus callosum. There were also multiple lacunes of the head of both caudate nuclei, anterior limb of the internal capsules, white matter, basal ganglia and thalami. The mutism akinetic was thought to be the result of a bilateral disruption of a functional loop including on each side, the supplementary motor area, the cingulate gyrus, the subcallosal tract and the head of the caudate nucleus. On the right side, the lesion of the caudate nucleus could have interrupted this loop normally involved in the induction of voluntary movements and in the communication with the external surroundings.

Twenty six patients with vascular dementia were studied. Five of them only, were referred for a cognitive decline and all the others because of focal neurological symptoms or a stroke. Twelve patients had a previous history of stroke and 21 an history of high blood pressure. Twenty three patients had gait disturbances. CT scanner and MRI showed a large proportion (23 patients) of lacunar or small sub-cortical strokes. Leuko-araiosis was present in 21 patients and cortical stroke only in 6. Finally, the lack of information concerning the onset and the course of the cognitive decline in 12 patients explain the difficulties to fulfill the criteria in some diagnostic evaluation scores particularly those of the DSM III R.

Vascular dementia is most often the result of multiple lesions affecting deep brain structures and the white matter. Diagnosis sometimes appears much simpler than it really is. Indeed, it is difficult to evaluate the impairment of higher brain functions and even to affirm dementia. Although the definition of dementia is simple theoretically, in clinical practice it is sometimes particularly difficult to assess when neurological impairments cause a socio-professional handicap. Two pitfalls should be avoided. First, a patient with signs of mental deficiency and a vascular lesion of brain vessels so easily identified by CT scan or MRI does not necessarily have vascular dementia. Secondly and inversely, dementia could be missed in a patient with a physical handicap whose defective mental functions go unnoticed both by his family and physician. Unlike Alzheimer's disease where neuropsychological problems predominate because these patients retain good physical autonomy for a long time, patients with vascular dementia are not explored routinely for neuropsychological disorders which may be hidden by more obvious neurological symptoms. Such disorders, especially gait disorders, are however the key to diagnosis. Mixed dementia is a third pitfall. This concept is based on histological findings and should not be used as a "catch-all" category. During the patient's lifetime diagnosis is probably impossible; current clinical scales do not take it into consideration.