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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The frequency of cerebral and cerebellar atrophy was assessed by computerized tomography (CT) in 26 heavy drinkers. Findings were correlated with clinical deficits, with the results of psychometric testing using the Wechsler Adult Intelligence Scale (WAIS), and with the alcoholic history and nutritional status. Cerebral atrophy was present in 19 cases (73%), 16 of whom also had cerebellar atrophy. There was a good correlation between the degree of cerebral hemisphere atrophy and age and length of drinking history, but a poor correlation between neurological deficits and atrophy. Impairment of visuo-spatial and visuo-motor functions with sparing of other non-dominant hemisphere functions and of verbal skills was the characteristic pattern found with the WAIS in 18 subjects; four showed a more global depression of intellectual function. The degree of cerebral hemisphere atrophy correlated significantly with the impairment of non-dominant hemisphere functions but not with total IQ.
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PMID:Brain atrophy and intellectual impairment in heavy drinkers--a clinical, psychometric and computerized tomography study. 27 64

A clinical and neuropsychological syndrome for early recognition of occult hydrocephalus and cerebral atrophy is described. Five illustrative patients are reported. The main features of the syndrome are (i) subjective non-specific complaints (headaches, depression and loss of memory); (ii) the tonic foot response of the sole and the grasp reflex of the foot in the absence of the grasp reflex of the hand; (iii) attacks of sudden and transient loss of muscle tone in both lower limbs leading to falls without warning while standing or while walking. These attacks indistinguishable from drop-attacks are termed chalastic fits; (iv) a dissociation between the satisfactory performances on the Ottawa-Wechsler scale and the poor performances on Kohs Block Design test. Clinical and neuropsychological findings could not differentiate between occult hydrocephalus and cerebral atrophy; only radionuclide cisternography and computerized tomography were able to delineate the final diagnosis.
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PMID:A syndrome of early recognition of occult hydrocephalus and cerebral atrophy. 91 52

Neurological dysfunction, seizures and brain atrophy occur in a broad spectrum of acute and chronic neurological diseases. In certain instances, over-stimulation of N-methyl-D-aspartate receptors has been implicated. Quinolinic acid (QUIN) is an endogenous N-methyl-D-aspartate receptor agonist synthesized from L-tryptophan via the kynurenine pathway and thereby has the potential of mediating N-methyl-D-aspartate neuronal damage and dysfunction. Conversely, the related metabolite, kynurenic acid, is an antagonist of N-methyl-D-aspartate receptors and could modulate the neurotoxic effects of QUIN as well as disrupt excitatory amino acid neurotransmission. In the present study, markedly increased concentrations of QUIN were found in both lumbar cerebrospinal fluid (CSF) and post-mortem brain tissue of patients with inflammatory diseases (bacterial, viral, fungal and parasitic infections, meningitis, autoimmune diseases and septicaemia) independent of breakdown of the blood-brain barrier. The concentrations of kynurenic acid were also increased, but generally to a lesser degree than the increases in QUIN. In contrast, no increases in CSF QUIN were found in chronic neurodegenerative disorders, depression or myoclonic seizure disorders, while CSF kynurenic acid concentrations were significantly lower in Huntington's disease and Alzheimer's disease. In inflammatory disease patients, proportional increases in CSF L-kynurenine and reduced L-tryptophan accompanied the increases in CSF QUIN and kynurenic acid. These responses are consistent with induction of indoleamine-2,3-dioxygenase, the first enzyme of the kynurenine pathway which converts L-tryptophan to kynurenic acid and QUIN. Indeed, increases in both indoleamine-2,3-dioxygenase activity and QUIN concentrations were observed in the cerebral cortex of macaques infected with retrovirus, particularly those with local inflammatory lesions. Correlations between CSF QUIN, kynurenic acid and L-kynurenine with markers of immune stimulation (neopterin, white blood cell counts and IgG levels) indicate a relationship between accelerated kynurenine pathway metabolism and the degree of intracerebral immune stimulation. We conclude that inflammatory diseases are associated with accumulation of QUIN, kynurenic acid and L-kynurenine within the central nervous system, but that the available data do not support a role for QUIN in the aetiology of Huntington's disease or Alzheimer's disease. In conjunction with our previous reports that CSF QUIN concentrations are correlated to objective measures of neuropsychological deficits in HIV-1-infected patients, we hypothesize that QUIN and kynurenic acid are mediators of neuronal dysfunction and nerve cell death in inflammatory diseases. Therefore, strategies to attenuate the neurological effects of kynurenine pathway metabolites or attenuate the rate of their synthesis offer new approaches to therapy.
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PMID:Quinolinic acid and kynurenine pathway metabolism in inflammatory and non-inflammatory neurological disease. 142 88

This is a description of a computerized tomographic study of 45 non-delusional depressed, 29 delusional depressed patients and 77 neurotic control subjects. The cerebral atrophy ratio (CAR) on the three different slices and the ventricular ratio (VBR) of the anterior horn and the body of the lateral ventricles were calculated, analyzed and compared using Student's t test. Compared to the control subjects, the non-delusional depressive patients had greater CAR values than the controls but there were no significant differences of VBR values between the two groups. The patients with delusional depression had significantly larger CAR and VBR values than the non-delusional depressives and control subjects. The delusional depressives had greater brain atrophy than the non-delusionals and it was suggested that organic cerebral factors may have etiological significance in the depressions, especially the delusional depressives.
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PMID:A computerized tomographic study in patients with delusional and non-delusional depression. 163 38

We report an autopsy case of a 73 year-old female with idiopathic parkinsonism, characterized pathologically by the wide spread appearance of Lewy bodies (LBs) not only in the pigmented neurons in the midbrain and brainstem but also in the cerebral cortex. Initial symptoms at the age of 62 were finger tremor and gait disturbance, which were followed mainly by mental deterioration, such as regression, dependency, auditory hallucination, depression, emotional incontinence, and a personality change. In the terminal stage, nuchal stiffness in extension, one of the hallmarks of progressive supranuclear palsy, and slow and generalized tremor in all 4 extremities were noted. She died of aspiration pneumonia. The brain was somewhat small and weighed 1100 g after the fixation by formalin. Macroscopical findings included mild cerebral atrophy with mild pial thickening both in the frontal and temporal lobes and slight expansion of the ventricular system. Histopathologically, severe loss of neuronal cells in both the pallidum and Luy's body and moderate loss of large cells in the putamen were noted in addition to the typical findings of Parkinson's disease in the substantia nigra and locus caeruleus including neuronal cell loss, depigmentation, and gliosis. These findings in the basal ganglia were more conspicuous than the two controls of classical Parkinson's disease. The distribution, stainability in the routine methods of staining, and shape of Lewy bodies in the cerebral cortex conformed to those of previous reports. The similar case reports in the literatures do not seem to have paid much attention to the findings of the basal ganglia observed in our case.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[An autopsy case of idiopathic parkinsonism with numerous Lewy bodies in the cerebral cortex--diffuse Lewy body disease]. 165 48

Bit-mapped multicomponent CNV complex and reaction time (RT) were recorded and measured in 24 presenile patients with initial symptoms of very mild to moderately severe primary mental deterioration without depression, and in 10 age-matched controls. All patients underwent CT and MRI examinations, EEG spectral analysis and a battery of psychometric test. Significant group differences were obtained for measures of some post-S1 ERP and CNV components, particularly of the post-S1 N1b, P300 and early and late pre-S2 CNV. P300 with increased latency, no significant CNV activity, very prolonged RTs, EEG slowing down and diffuse brain atrophy were observed in the majority of patients with probable presenile Alzheimer's dementia. These results suggest that CNV/RT and EEG activity changes similar to those observed in our patients may constitute a valuable clue for the study of brain dysfunction in the early stage of presenile idiopathic cognitive impairment.
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PMID:Effect of physiological and pathological aging processes on topographic bit-mapped cognitive evoked potentials in presenile subjects. 180 55

Nineteen cases are described, including 12 cases from three different families and 7 nonfamilial cases, in which multisystem neurological disease was associated with acanthocytosis in peripheral blood and normal plasma lipoproteins. Mild acanthocytosis can easily be overlooked, and scanning electron microscopy may be helpful. Some neurologically asymptomatic relatives with significant acanthocytosis were identified during family screening, including some who were clinically affected. The mean age of onset was 32 (range 8-62) yrs and the clinical course was usually progressive but there was marked phenotypic variation. Cognitive impairment, psychiatric features and organic personality change occurred in over half the cases, and more than one-third had seizures. Orofaciolingual involuntary movements and pseudobulbar disturbance commonly caused dysphagia and dysarthria that was sometimes severe, but biting of the lips or tongue was rarely seen. Chorea was seen in almost all symptomatic cases but dystonia, tics, involuntary vocalizations and akinetic-rigid features also occurred. Two cases had no movement disorder at all. Computerized tomography often demonstrated cerebral atrophy. Caudate atrophy was seen less commonly, and nonspecific focal and symmetric signal abnormalities from the caudate or lentiform nuclei were seen by magnetic resonance imaging in 3 out of 4 cases. Depression or absence of tendon reflexes was noted in 13 cases and neurophysiological abnormalities often indicated an axonal neuropathy. Sural nerve biopsies from 3 cases showed evidence of a chronic axonal neuropathy with prominent regenerative activity, predominantly affecting the large diameter myelinated fibres. Serum creatine kinase activity was increased in 11 cases but without clinical evidence of a myopathy. Postmortem neuropathological examination in 1 case revealed extensive neuronal loss and gliosis affecting the corpus striatum, pallidum, and the substantia nigra, especially the pars reticulata. The cerebral cortex appeared spared and the spinal cord showed no evidence of anterior horn cell loss. Two examples of the McLeod phenotype, an X-linked abnormality of expression of Kell blood group antigens, were identified in a single family and included 1 female. The genetics of neuroacanthocytosis are unclear and probably heterogeneous, but the available pedigree data and the association with the McLeod phenotype suggest that there may be a locus for this disorder on the short arm of the X chromosome.
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PMID:Neuroacanthocytosis. A clinical, haematological and pathological study of 19 cases. 199 79

Eight patients are reported who shared the combination of bilateral basal ganglia lesions and a frontal lobe-like syndrome. The main features were inertia and loss of drive, with preservation of intellectual function. Some patients showed stereotyped activities with compulsive and obsessive behaviour which were sometimes highly elaborate in pattern. Extrapyramidal clinical signs were absent or mild. Brain damage, related to anoxic or toxic encephalopathy, was demonstrated by CT scans and MRI. The lesions appeared to be confined to the lentiform nuclei, particularly affecting the pallidum, although there was generalized brain atrophy in 2 cases. Positron emission tomography (PET) in 7 patients revealed hypometabolism of the prefrontal cortex relative to other parts of the brain. The PET studies suggest dysfunction of the prefrontal cortex as a result of damage to the lentiform nuclei. These clinical, anatomical and functional observations emphasize the role of the circuits linking the prefrontal associative cortex and some specific areas of the neostriatum, including the pallidum. The existence of distinct nonoverlapping circuits in the motor field or in the associative field can explain the fact that basal ganglia lesions may give rise to a clinical picture that is either purely motor, purely behavioural (as in some of our patients), or both. Similarities existed between some symptoms found in our patients and certain features of major psychiatric illnesses such as severe depression, catatonic schizophrenia, and obsessive-compulsive disorder. This raises the hypothesis that some aspects of these psychiatric disorders could be related to structural and physiological disturbances in the systems linking the frontal associative cortex and the basal ganglia.
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PMID:Obsessive-compulsive and other behavioural changes with bilateral basal ganglia lesions. A neuropsychological, magnetic resonance imaging and positron tomography study. 278 40

The distribution of cerebral blood flow and metabolism is related to neuronal activity. Cerebral blood flow (CBF), cerebral metabolic rate of oxygen (CMRO2), and oxygen extraction fraction (OEF) in ten patients with Parkinson's disease and five age-matched normal control subjects were measured with positron emission tomography (PET) using 15O2, C15O2 steady state inhalational technique to investigate functional changes of the cortex and the basal ganglia in Parkinson's disease. All patients had no history of cerebrovascular disease and CT scan showed no abnormal findings except for moderate cerebral atrophy in only one patient. When the level of clinical disability was related on the scale of Hoehn and Yahr, one patient was stage I, four were stage II, four were stage III, and one was stage IV. Psychic symptoms which include hallucination, depression, and dementia were recognized in four patients. One of these four patients was mildly demented. Four patients were newly diagnosed and had never been treated with antiparkinsonian medication before. Before the patients had their PET study their antiparkinsonian medication was discontinued for more than three days. But in two patients PET study was performed without discontinuity of antiparkinsonian medication. The values for regional CBF and regional CMRO2 were lower in the patients than in the normal control subjects, especially in the frontal cortex there was a significant decrease of CBF and CMRO2. There was no discrepancy between CBF and CMRO2 both in the patients and the normal control. CBF and CMRO2 in the cortex and the basal ganglia were not correlated with the severity of tremor, bradykinesia, and rigidity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Cerebral blood flow and oxygen metabolism in patients with Parkinson's disease]. 326 73

The Acquired Immune Deficiency Syndrome (AIDS) has been associated with a series of central nervous system (CNS) complications, including focal and nonfocal neurological indications. Overall, the most common form of CNS dysfunction is diffuse cerebral atrophy pathologically characterized by neuronal loss, glial nodules, and microfocal demyelination. Consequent neuropsychological deficits present an insidious course initially typified by poor memory and concentration, along with psychomotor retardation and blunted affect which resembles psychological depression. Gradually over several weeks to months, patients exhibit marked global cognitive impairment and can become severely disoriented and delusional. Clinical research relevant to these CNS complications and neuropsychological sequelae are reviewed.
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PMID:Acquired immune deficiency syndrome: an overview of central nervous system complications and neuropsychological sequelae. 353 45


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