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Query: UMLS:C0085632 (apathy)
 4,089 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A simple, semiquantitative paper chromatographic method was used to identify samples of cerebrospinal fluid containing elevated concentrations of myo-inositol. All patients whose CSF inositol concentrations were greater than 70 mug/ml (as determined by S. carlsbergensis microbiological assay) showed disturbances of the state of consciousness, reported as stupor, coma or confusion in adults, or apathy and stupor in infants. An elevated level of inositol in cerebrospinal fluid appeared to be a characteristic finding in infants under one year of age. Among other age groups no common etiology was correlated with high inositol concentration.
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PMID:Elevated myo-inositol concentrations in cerebrospinal fluid of neonates and of patients with an impaired state of consciousness. 101 79

Magnesium is an essential cofactor for many enzymatic reactions, especially those involved in energy metabolism. Deficits of magnesium are prevalent due to inadequate intake or malabsorption and due to the renal loss of magnesium that occurs in certain disease states (alcoholism, diabetes) and with drug therapy (diuretics, aminoglycosides, cisplatin, digoxin, cyclosporin, amphotericin B). Protracted deficits of magnesium in humans and animals result in neurological disturbances, including hyperexcitability, convulsions and various psychiatric symptoms ranging from apathy to psychosis, some of which can be reversed with magnesium supplementation, others requiring correction of the dysregulation mechanism. Although the role of magnesium in neuronal function is not completely understood, a lowering of CSF or brain magnesium can induce epileptiform activity and there is an association between decreased CSF magnesium and the development of seizures. CSF concentrations of magnesium are normally higher than magnesium plasma ultrafiltrate (diffusible) concentrations due to the active transport of magnesium across the blood-brain barrier. Under conditions of magnesium deficiency, CSF concentrations decline, although this decline lags behind and is less pronounced than the changes observed in plasma magnesium concentrations. Decreases in CSF magnesium concentrations correlate with the alterations observed in extracellular brain magnesium concentrations in animals following the dietary deprivation of magnesium. CSF magnesium concentrations can readily be repleted following magnesium supplementation, although high dose magnesium therapy, such as that used in the treatment of convulsions in eclampsia, will only increase CSF magnesium concentrations to a very limited degree (approximately 11-18 per cent) above physiological concentrations. Greater increases in CSF magnesium may occur in neonates since neonatal swine, following treatment with magnesium, have CSF magnesium concentrations that are similar to their plasma concentrations. There has been a recent resurgence of interest in magnesium deficiency and its neurological consequences due to the finding that magnesium, at physiological concentrations, blocks N-methyl-D-aspartate (NMDA) receptors in neurones. NMDA receptors are normally activated by glutamate and/or aspartate which represent the principal neurotransmitters for excitatory synaptic transmission in vertebrate CNS. Magnesium deficiency produces epileptiform activity in the CNS which can be blocked by NMDA receptor antagonists. Other mechanisms, including alterations in Na+/K(+)-ATPase activity, cAMP/cGMP concentrations and calcium currents in pre- and postsynaptic membranes, may also be at least partially responsible for the neuronal effects associated with low brain magnesium. Further studies are necessary to increase our understanding of the neurological implications of magnesium deficit in the central nervous system.
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PMID:Brain and CSF magnesium concentrations during magnesium deficit in animals and humans: neurological symptoms. 129 67

We describe 2 new patients from a family in which 10 persons in 3 successive generations had a dominant neuropsychiatric disorder characterized by apathy, central hypoventilation, and parkinsonism. Neuropathologically, both patients showed severe neuronal loss and reactive gliosis in the substantia nigra. Neurochemical studies showed a marked depletion of dopamine in substantia nigra, putamen, and caudate nucleus, as well as reduction in serotonin content in the substantia nigra. Glutamate contents were low in frontal cortex and thalamus, and gamma-aminobutyric acid (GABA) contents were low in thalamus and substantia nigra of both patients. In addition, phosphoethanolamine contents were reduced in all brain regions of both patients, especially in the substantia nigra. One patient with severe symptoms had low levels of homovanillic acid, 5-hydroxyindoleacetic acid, and GABA in his CSF repeatedly for 3 years before death (aged 58), while the 2nd patient died (aged 51) of an unrelated cause before developing any symptoms of the familial disorder. Because brain deficiencies of multiple neurotransmitters appear to be involved, this disorder is unlikely to respond to treatment; however, neurochemical studies of CSF may make presymptomatic diagnosis feasible.
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PMID:Dominantly inherited apathy, central hypoventilation, and Parkinson's syndrome: clinical, biochemical, and neuropathologic studies of 2 new cases. 224 38

The paper describes the psychiatric status on the basis of 76 patients with acquired immune deficiency syndrome. There is considerable difference between the different stages of the disease. The disorders are divided into groups following the German and French psychopathological tradition, where the incidence is dependent on the underlying complaint. 50% of the patients suffered from chronic psychoorganic disorders (34% organic personality disorders, 16% dementia). 9% suffered from an acute psychosis caused by complications and founded on substantial physical illness. 3 patients showed symptoms of a (under given circumstances) hitherto unknown endoform psychosis. In 9% of the patients, psychoreactive disturbances (anxiety and reactive depression) were observed. Two infants had congenital development deficiencies. 25% of the patients were without any psychopathology. Patients showing organic personality disorders mostly resemble each other to such a degree as to form a separate group. We suggest to name this group according to the most prominent psychopathology as "AIDS-lethargy". This status is characterised by a specific apathy, tiredness and indolence of the patients combined with the lack of emotional participation related to their own destiny. AIDS-lethargy is the first manifestation in appearance of the HIV infection of the brain itself. Another sequel of the brain infection is AIDS dementia which can be classified as "subcortical dementia" and differs from the more current forms of dementia clinically. Affected are mainly neuropsychologic functions like arousal, attention, mood and motivation, whereas the hallmarks of cortical involvement-aphasia, agnosia and apraxia-are not present. Supplementary findings (EEG, CCT, CSF): The group of patients with chronic psychoorganic disorders differs significantly from the group with psychoreactive disorders and normals. Pathological EEG and CCT are more frequent in psychoorganic disorders. CSF-test-including the intrathecally synthesized antibodies against HIV-does not show traceable variation in either group. There are four problems which may be combined in a given acute psychopathological HIV-syndrome: 1. Being member of a risk group with its reactive, psychosocial and personality problems. 2. Individual mental and emotional reaction to the fact of infection 3. Chronic psychoorganic disturbances. 4. Acute organic psychoses as a result of complications and other physical illness.
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PMID:[Psychopathologic pictures in HIV infection: AIDS lethargy and AIDS dementia]. 340 94

A man aged 56 years, previously healthy, developed asthenia, hypersonnia, apathy, later polydipsia and bulimia, headache and episodes of unconsciousness. There was temporary improvement with steriod therapy, but ever-deepening stupor appeared till death due to bronchopneumonia. All blood chemistry examinations were normal. The CSF IgG was elevated but no neoplastic cells were seen. At autopsy areas of grayish color in the basal gagnlia and granulomatous tissue in the floor of the third ventricle and in the mamillary bodies were seen, and the gonads were attrophied. Microscopically, in the floor of third ventricle, mamillary bodies and adjacent leptomeninges there was granulomatous tissue made up of more-or-less typical cells of the reticulum, polymorphonuclear cells, plasma cells and some phagocytes along with proliferation of small blood vessels and reticulin fibers. In addition, the white matter of the frontal lobes, pons, middle cerebellar peduncle and cerebellar white matter contained diffuse proliferation of pleomorphic histiocytic elements with questionable atypical mitoses. Notwithstanding, the morphology of our case suggests that it is a peculiar form of malignant reticulosis (or malignant histocytosis) related to histiocytosis X. The duplicity of the features of our case suggests it to be neoplastic, where the proliferative phase is followed by a granulomatous and sclerotic one.
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PMID:A peculiar case of malignant cerebral reticulosis: clinico-pathological study. 615 91

A 16-year-old boy had congenital absence of pain sensitivity and no impairment of other sensory modalities. Routine electrophysiologic investigation showed no abnormalities. The threshold and latency of electrically elicited corneal reflex and cortical potentials evoked by tooth pulp stimulation were normal, but suprathreshold electric stimulation of corneal mucosa and dental pulp, as well as electric stimulation of dorsal roots, did not elicit pain. The total CSF opioid activity was raised. However, naloxone hydrochloride administration failed to reverse the analgesia. The axon reflex to intradermal injection of histamine dihydrochloride was absent. Cutaneous nerve branches showed unspecific changes affecting part of unmyelinated axons. most of the unmyelinated as well as the myelinated axons were normal. We consider the case an example of congenital indifference to pain.
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PMID:Congenital absence of pain. 616 87

Three children, from different kinships, with generalized insensitivity to pain, showed unusual manifestations of congenital, presumably inherited, sensory and autonomic neuropathy. The first child appeared to have a syndrome resembling those previously described as congenital indifference to pain, congenital universal loss of pain sensation from infancy without other apparent neurological deficit. Unlike most types of hereditary sensory and autonomic neuropathies (types I, II, III), but like type IV, she had normal sensory nerve action potentials. Abnormalities of sudomotor function and of somatosensory evoked potentials were demonstrated. A severe decrease in the number of sural nerve A delta fibres and a small reduction in C fibres were demonstrated morphometrically. An abnormality of C fibres was confirmed by a marked reduction in nerve dopamine-beta-hydroxylase activity. The plasma and CSF concentrations of beta endorphins, substance P and several other neuropeptides and hormones were normal. Unequivocal evidence of a neuropathic lesion is provided by this patient; her disorder may be identified as the fifth type of hereditary sensory and autonomic neuropathy. The second patient had a congenital pansensory neuropathy and progressive retinitis pigmentosa. Whether the disorder is inherited and, if so, whether the retinitis pigmentosa results from the same or from a second genetic abnormality, is unclear. The third case has, in addition to what is usually seen in hereditary sensory and autonomic neuropathy, type II, an unusually severe kinaesthetic difficulty in oral food handling. The sural nerves of the second and third patients had fibre composition characteristic of hereditary sensory and autonomic neuropathy, type II, few or no myelinated fibres and reduced numbers of unmyelinated fibres.
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PMID:Not 'indifference to pain' but varieties of hereditary sensory and autonomic neuropathy. 618 47

CSF from a patient with congenital indifference to pain was found to produce analgesia in the rat following intracerebroventricular injections. The analgesic effect was attenuated by pretreatment with naloxone suggesting the involvement of hyperactive endogenous opiate mechanisms in this patient.
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PMID:Intracerebroventricular injection of cerebrospinal fluid (CSF) from a patient with congenital indifference to pain induces analgesia in rats. 621 Feb 10

HIV-associated neurological manifestations: dementia, myelopathy, and neuropathy, have become one of the commonest causes of neurological disorders in young people. Cognitive impairment develops in about 30 p. 100 of patients with AIDS and frank dementia in 15 to 20 p. 100 with an annual incidence after AIDS of approximatively 7 p. 100. Typically, the onset of dementia is relatively abrupt over a few weeks or months. The clinical manifestations of the encephalopathy now termed "HIV-dementia", suggest predominant subcortical or frontal involvement. Typical presentation includes apathy and inertia, memory loss and cognitive slowing, minor depressive symptoms and withdrawal from usual activities. Neurological examination may show hypertonia of lower limbs, tremor, clonus, frontal release signs and hyperactive reflexes. Terminally, the patient is bedbound, incontinent, abulic or mute with decorticate posturing leading to death over 3 to 6 months. However, a stabilisation and even a regression of the cognitive disorders have been observed following antiretroviral treatment. Radiological features of HIV dementia include both central and cortical atrophy and white matter rarefaction. However they are neither invariable nor specific. Together with CSF examination, they are more important to exclude opportunistic infections. Indeed, although a completely normal CSF profile may reasonably exclude the diagnosis; at present, no single test or combination of tests can reliably diagnose HIV dementia. Although the clinical characteristics of HIV-dementia are now clearly established, its pathogenesis is unclear and its pathological counterpart remains a matter of debate. A number of "HIV-induced" lesions may be found in the brain of AIDS patients and their causative role in HIV-dementia has been considered. They include HIV encephalitis due to productive CNS infection by the virus, diffuse white matter pallor "HIV-leukoencephalopathy" reflecting an abnormality of the blood brain barrier, involvement of the grey matter, "diffuse poliodystrophy", with neuronal loss that results, at least partly, from a process of programmed cell death and axonal damage. These changes are variably associated in patients with HIV dementia, however none of them can be closely related to the cognitive disorders. This suggests that the neuronal dysfunction underlying HIV-dementia results from different mechanisms that are variably associated and may interact mutually. These include production of viral proteins, microglial activation with consequent production of neurotoxic factors such as proinflammatory cytokines, free radicals, derivates of arachidonic acid, or quinoleic acid, and blood borne neurotoxic factors in particular cytokines.
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PMID:[Dementia and human inmmunodeficiency virus infection]. 983 49

The patient, a 65-year-old woman, had liver cirrhosis, and had blood transfusion at the age of 49 and 56. Early in September, 1989, she gradually developed numbness of the legs, staggering gait, and apathy with hallucination. In October, she became incontinent and unable to stand, and was admitted to Konan Hospital. On admission, she was disoriented with poor comprehension. Cranial nerves were intact except for horizontal nystagmus on lateral gaze. She had generalized areflexia without pathological reflex. Muscular forces were fairly preserved. Superficial sensations were diminished in the upper limbs as well as below Th-7 level. Deep sensation was abolished in the distal parts of the extremities with athetotic finger postures on arm rising. She had urinary and fecal incontinence. Results of routine laboratory examinations were non-contributory. Chest CT scan and sputum cytology were normal. CSF contained one cell/microliter, 95 mg/dl of protein with positive oligoclonal IgG bands. Anti-HTLV-I antibody was positive in serum and CSF. Urodynamic studies showed neurogenic bladder of supranuclear type. MNCV was slightly decreased. SNAP and SEP were not evoked. On sural nerve biopsy, the density of myelinated fibers was 720/mm2, and that of unmyelinated fibers, 26,978/mm2. ABR and VEP were abnormal. EEG showed diffuse theta waves with paroxysmal delta and sharp waves. T2-weighted MR images of the brain showed patchy areas of high signal intensity in the cerebral white matter. Soon after administration of methylprednisolone, her consciousness became clear. EEG normalized in 4 months. Twenty months after the onset, she became ambulant with crutch, but still has dysuria and sensory deficits in the hands and lower limbs. The possible relationship between encephalomyeloneuritis and HTLV-I infection was discussed.
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PMID:[A case of encephalomyeloneuritis and HTLV-I infection]. 1047 58


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