Rivista di patologia nervosa e mentale最新文献

Although more than twenty-five years of clinical use and several placebo-controlled studies have demonstrated the clinical effectiveness of anti-depressant drugs, the mechanism through which these drugs function and how they relate to the pathological mechanisms that underlie depressive disorders are still not clear. The present article briefly reviews the literature available on the subject. In chronological order, it examines studies on the clinical effectiveness of antidepressants, their effects on biogenic amine metabolism and on known receptor systems. The existence of possible specific receptor systems for tricyclic anti-depressants, their modifications during depressive illness, the effect of treatment with psychotropic drugs and the role which these systems may play in depression are then illustrated.

Several subjects who tell their depression and play a part of it in front of the doctor without being really depressed are reported. Some of them try to hide the symptoms (irritability or erethism, ceremonials of obsessive neurosis, shunning of phobia) which, in their opinion, might be detrimental to their reputation. Others neglect to describe some of the symptoms of their polymorphous clinical picture only underlining the depressive signs. Some others play a part of depression because they have believed to recognize themselves in persons presented by mass media, because it seems to them a duty to show an adequate depression in case of mournful event, or because they "convert" their problem into a depression. Some others use depression as a blackmail, or to obtain an advantage from doctor's conviction about their illness. The reason for the high frequency of similar cases in the present time are examined: the scientific divulgation and the acceptance of depression by the modern society are among the most important ones. The peculiar semantic vicissitudes of the word depression are also reviewed. A widening of the boundaries of depression has contributed to an increase in the number of the cases. Finally, in addition to patients who are depressed without being aware of it, the authors focus the inverse possibility: patients who believed or try to make their doctor believe (playing the part of depression in front of them) that they are depressed.

A case of unusual Neuro-Behçet syndrome is reported. Four years of follow-up revealed at beginning later the occurrence of acute meningoencephalitis caractherized by two convulsive fits. CSF examination revealed high albumin and cells contents. CT examination of the head was negative. Incomplete clinical improvement was obtained by using steroids. Differential diagnosis is finally discussed.

A case of intracranial multiple aneurysms associated with a giant arteriovenous malformation is reported. Three aneurysms were found arising from the arteries feeding the malformation. The patient could not be operated because of his age, neurological condition and the size of the arteriovenous malformation. Previously reported cases of cerebral aneurysms associated with arteriovenous malformation are reviewed. Our case well illustrates the possible role of hemodynamic stresses induced by the malformation on the development of the aneurysms.

This report describes an 18-year-old woman who, after a febrile illness, developed opsoclonus, truncal ataxia and mild body tremulousness. The oculomotor disorder was documented by electro-oculography. The results of extensive neurological investigations, including CT scan, visual, auditory and somesthetic evoked potentials, nuclear magnetic resonance and complete cerebrospinal fluid evaluation, were negative. The patient recovered completely within about 1 month. After having thoroughly analyzed the pertinent literature, we conclude that the pathogenetic hypothesis of direct encephalitic damage is unproved, and that these peculiar unwanted ocular movements can be explained by assuming an abnormality of "pause" cell control over saccadic "burst" neurons.

An unusual case of Chiari type I malformation is presented. The only symptom was a "drop attack" during sneezing or coughing. The possible pathogenetic mechanisms are briefly reviewed and the good results of the surgical therapy are stressed.

Auditory and somatosensory evoked potentials were recorded from 10 patients suffering from Friedreich's ataxia. All patients were subjected to audiological tests and EMG-ENG study. Acoustic evoked potentials recordings included brainstem acoustic evoked potentials and long latency components. Peripheral and central components of somatosensory evoked potentials were obtained by stimulating the median nerve at the wrist and elbow. Various abnormalities of the cortical components were observed in all patients for both acoustic and somatosensory evoked potentials. Analysis of brainstem acoustic evoked potentials and of the early components of somatosensory evoked potentials showed a different incidence of abnormalities. The main feature of brainstem acoustic evoked potential changes was the frequent absence of one or more waves; the greatest abnormalities occurred in patients whose disease was of long duration. Long latency components (N85) were significantly prolonged in all but one patient. There was often an absence or reduction of early somatosensory evoked potentials with normal or near normal latencies, even though cortical responses were markedly prolonged. The sensory conduction velocity between stimulation sites at wrist and elbow was normal in all patients. Clinically brainstem acoustic evoked potentials may prove to be a reliable means of monitoring the progression of the disease, while long latency components and somatosensory evoked potentials could be used as complementary procedures in early diagnosis.

A prospective study of head injury patients was carried out in the city of Ravenna in 1984. A complete record was completed for all patients admitted for hospital care. More than 50 clinical and diagnostic variables were evaluated to investigate risk factors on patients admitted to a Non-Neurosurgical Unit with CT facilities. Our report deals with 578 cases and shows some interesting findings: The mortality in the entire trauma-group was 42 cases; 35 (83%) of these died immediately after the accident or while being transported to the hospital. The number of patients hospitalized (42%) was much higher than that in previous reports concerning hospital admission of head injury patients. 9 cases were sent from the First Aid to Regional Neurosurgical Centre (Bellaria Hospital, Bologna). Among the other patients admitted to the Non-Neurosurgical Centre, 12 showed cerebral lesions on the CT (1 extradural haematoma). Risk factors were evaluated by comparing EEG, skull fractures and poor clinical condition with the presence of cerebral lesions. Our data show a peculiar situation here in Italy: a large number of hospital admissions for minor head injuries, of whom relatively few patients are at risk of intracranial post-traumatic haematoma.

Thirteen patients affected by either dominant or recessive and/or sporadic olivopontocerebellar atrophy were studied. All patients were subjected to auditory evoked potential recordings including early and long latency components, CT scans, vestibular and EMG-ENG examinations. In nine patients somatosensory evoked potentials were also recorded. Clear-cut abnormalities in brainstem auditory evoked potentials were observed in only two patients while a slight reduction of the IV-V/I amplitude ratio was found in seven cases. N85 was increased in two patients. The main feature of somatosensory evoked potentials abnormalities was a delayed N20 in association with prolonged N13-N20 central conduction time (five patients). For all patients the CT scan varying degrees of cerebellar and brainstem atrophy. There was no clear correlation between the abnormalities revealed by neurophysiological and neuroradiological investigations and the severity and duration of the illness. It is noteworthy that auditory and/or somatosensory evoked potential changes were found in all dominant olivopontocerebellar atrophy patients.

The author describe a patient with bilateral giant aneurysms of the internal carotid artery in the region of the ophthalmic artery. These lesions are very rare and can be mistakenly diagnosed as intracranial tumors on the basis of the clinical presentation and CT findings alone. The correct diagnosis is made via cerebral panangiography and a successful surgical treatment for this pathology is often available.