1/22. Reversible delayed leukoencephalopathy following intravenous heroin overdose.We present serial neuropsychological, magnetic resonance (MR) imaging and EEG changes in a case of widespread CNS myelinopathy due to intravenous heroin overdose complicated by a period of prolonged unconsciousness. Following recovery from the acute overdose, the subject had the delayed onset of akinetic mutism with urinary incontinence. Sequential formal neuro-psychological assessments over 9 months showed evolution from severe global cerebral dysfunction to moderate disturbance of frontal lobe function. Almost complete resolution of diffuse white matter signal changes, accompanied by the development of a degree of volume loss, was evident on serial MR imaging over the same period, and generalized arrhythmic delta-range slowing on the EEG evolved int o a near normal pattern.- - - - - - - - - - ranking = 1keywords = unconsciousness, consciousness (Clic here for more details about this article) |
2/22. Recovery of children after severe head injury. Psychoreactive superimpositions.After the regaining of consciousness and awareness in the strange environment of an intensive care unit, an injured child is exposed to a situation of extreme psychological impact. This situation, in addition to a probably organically changed reactivity, is liable to provoke a particular, abnormal psychic response. The abnormal reaction can follow the pattern of a feigned-death response and thus mimic an organic coma vigile (apallic state). The resulting psychoreactive stuporous state ("Sleeping beauty syndrome") may lead to a misjudgement of the recovery degree and may delay early rehabilitation. With the help of a representative case, the clinical manifestation, course, and treatment of this reactive juvenile syndrome are presented. The interaction of physiogenic and psychogenic factors responsible for some psychiatric sequelae during the early period after head injury is emphasized.- - - - - - - - - - ranking = 0.01202928911344keywords = consciousness, state (Clic here for more details about this article) |
3/22. Chronic akinetic mutism after mesencephalic-diencephalic infarction: remediated with dopaminergic medications.OBJECTIVE: akinetic mutism (AKM) is an uncommon disorder with a complex neuropathology. There is no generally accepted treatment, and it is not known if late treatments are effective. The relationship between AKM and abulia is uncertain. methods: The effects of dopaminergic treatment of a patient with chronic AKM after discrete bilateral infarctions of the mesencephalic ventral tegmental area and the lateral hypothalamus were studied with motor measures, the Functional Independence Measure (FIM), and neuropsychological tests. RESULTS: Treatment with a combination of carbidopa/levodopa and pergolide produced prompt amelioration of AKM with dramatic and rapid improvement in FIM. An apathetic, amotivational state persisted despite resolution of akinesia and normal frontal executive functions. CONCLUSIONS: AKM may respond to dopaminergic treatment even after months of severe akinesia. The mechanism of abulia is more complex than simply a partial dopaminergic deficiency state and may persist even when AKM is treated and frontal cognitive functions are normal.- - - - - - - - - - ranking = 0.0004376418194729keywords = state (Clic here for more details about this article) |
4/22. akinetic mutism caused by bilateral infiltration of the fornix in a patient with astrocytoma.In a 59-year-old female patient, a world health organization (WHO) grade II astrocytoma had been diagnosed 16 years ago, which finally progressed into WHO grade III. Several right frontal neurosurgical resections, local radiation and a local radioimplant had been applied. Despite this long record, she was reported alert with a Karnofsky index of 90% until admission. Within a few weeks she rapidly developed akinetic mutism. Upon admission, computed tomography (CT) scan showed a large cystic right frontal defect and a suggested small tumor recurrence. White matter of the frontal lobe appeared to be translucent and compatible with previous radiation. The severe mental changes were initially attributed to a delayed radiation encephalopathy. Neuropathologically, the white matter of the frontal lobe showed mild elevated cell density consistent with gliosis; however, a tumor recurrence invading the tip of the corpus callosum and invading the entire length both fornices appeared. From the neuropathological findings of massive local tumor recurrence in both fornices, together with the acute clinical onset, it seems unlikely that the sequel of radiotherapy caused akinetic mutism, but the symmetric and severe involvement of the limbic system. We conclude that the rapid progression from a state of alertness to a full clinical picture of akinetic mutism was because of infiltration of both fornices.- - - - - - - - - - ranking = 0.00021882090973645keywords = state (Clic here for more details about this article) |
5/22. Residual cerebral activity and behavioural fragments can remain in the persistently vegetative brain.This report identifies evidence of partially functional cerebral regions in catastrophically injured brains. To study five patients in a persistent vegetative state (PVS) with different behavioural features, we employed [(18)F]fluorodeoxyglucose-positron emission tomography (FDG-PET), MRI and magnetoencephalographic (MEG) responses to sensory stimulation. Each patient's brain expressed a unique metabolic pattern. In three of the five patients, co-registered PET/MRI correlate islands of relatively preserved brain metabolism with isolated fragments of behaviour. Two patients had suffered anoxic injuries and demonstrated marked decreases in overall cerebral metabolism to 30-40% of normal. Two other patients with non-anoxic, multifocal brain injuries demonstrated several isolated brain regions with relatively higher metabolic rates, that ranged up to 50-80% of normal. Nevertheless, their global metabolic rates remained <50% of normal. MEG recordings from three PVS patients provide clear evidence for the absence, abnormality or reduction of evoked responses. Despite major abnormalities, however, these data also provide evidence for localized residual activity at the cortical level. Each patient partially preserved restricted sensory representations, as evidenced by slow evoked magnetic fields and gamma band activity. In two patients, these activations correlate with isolated behavioural patterns and metabolic activity. Remaining active regions identified in the three PVS patients with behavioural fragments appear to consist of segregated corticothalamic networks that retain connectivity and partial functional integrity. A single patient who suffered severe injury to the tegmental mesencephalon and paramedian thalamus showed widely preserved cortical metabolism, and a global average metabolic rate of 65% of normal. The relatively high preservation of cortical metabolism in this patient defines the first functional correlate of clinical- pathological reports associating permanent unconsciousness with structural damage to these regions. The specific patterns of preserved metabolic activity identified in these patients do not appear to represent random survivals of a few neuronal islands; rather they reflect novel evidence of the modular nature of individual functional networks that underlie conscious brain function. The variations in cerebral metabolism in chronic PVS patients indicate that some cerebral regions can retain partial function in catastrophically injured brains.- - - - - - - - - - ranking = 1.0002188209097keywords = unconsciousness, consciousness, state (Clic here for more details about this article) |
6/22. adult "failure-to-thrive" syndrome.The analogy between the "failure-to-thrive" syndrome of childhood and a symptom complex seen in adult neurology is described. Adults presenting with a variety of central nervous system diseases occasionally seem to follow an unusual stereotyped course resulting in intractable weight loss, wide variations in temperature, and a tendency to intractable decubitus ulcerations in a setting of decreased levels of consciousness. Sudden death occurs unexpectedly. This syndrome can be observed following cerebral thrombosis, traumatic encephalopathy, degenerative central nervous system disorders, and encephalitis. The pathophysiology is thought to result from the random aggregate of lesions rather than a verifiable discrete hypothalamic deficit.- - - - - - - - - - ranking = 0.011591647293967keywords = consciousness (Clic here for more details about this article) |
7/22. Event-related brain potentials in a patient with akinetic mutism.The clinical pattern of complete akinetic mutism (AM) was observed in a patient with a bilateral infarction of the anterior cerebral arteries extending to the rostral cingulate cortex and the supplementary motor areas. Since the patient was unable to produce any overt response, event-related brain potentials (ERPs) were used to obtain information about cortical processing of stimuli. Oddball tasks with simple acoustical stimuli and semantic categories were used. Verbal processing was further assessed by comparing event-related potentials to words compatible versus incompatible to the semantic context. Although the pattern of cortical responses was abnormal, differential responses were clearly obtained to semantically different word classes. Thus, the hypothesis about cortical non-responsivity of AM patients, drawn from several previous reports, was not supported. An ERP examination in AM patients can deliver information about their mental state, provided that the stimuli and tasks possess a wide range of informational complexity and motivational value.- - - - - - - - - - ranking = 0.00021882090973645keywords = state (Clic here for more details about this article) |
8/22. Preserved auditory cognitive ERPs in severe akinetic mutism: a case report.kinetic mustism is a dramatic deficit in spontaneous initiation of voluntary motor and speech acts, usually secondary to bilateral lesions of the anterior cingulate cortices and supplementary motor areas [Principles of neurology, McGraw-Hill, new york, 1989]. Given the obvious limitations of traditional neuropsychological testing in this clinical context, the use of neurophysiological tools such as bedside auditory cognitive event-related potentials (ERPs), recently proven to be relevant to evaluate comatose and vegetative patients [Clin. Neurophysiol. 110 (9) (1999) 1601; news Physiol. Sci. 17 (2002) 38], may constitute an interesting alternative. Here, we present the ERPs of a 38-year-old right-handed woman with severe akinetic mutism recorded in a passive auditory odd-ball paradigm. In spite of this severe clinical state, we could observe the presence of a "Mismatch Negativity", and of a larger P300 in rare trials than in frequent ones. By revealing a high level of cognitive integration of environmental auditory information, our study emphasizes the potential clinical relevance of MMN and P300 recordings in akinetic mutism to assess patient cognitive functioning.- - - - - - - - - - ranking = 0.00021882090973645keywords = state (Clic here for more details about this article) |
9/22. frontal lobe and cingulate cortical metabolic dysfunction in acquired akinetic mutism: a PET study of the interval form of carbon monoxide poisoning.A middle-aged man suffering from acute carbon monoxide intoxication was clinically assessed to be in an akinetic and mute state. In order to elucidate regional cerebral disturbances, brain metabolism was investigated with fluoro-deoxyglucose positron emission tomography ((18)FDG-PET) 5.5 months after intoxication. Significantly reduced metabolic rates of glucose were revealed in selected brain regions, especially in both the frontal and anterior cingulate cortices, as well as in the subcortical white matter. Frontal and cingulate cortices showed a preserved metabolism of 35-53%, whereas the regional glucose consumption in cerebral white matter was reduced by more than 70%. In contrast, other areas of the brain such as the sensory-motor cortex, parts of the temporal lobes, basal ganglia and brainstem disclosed normal metabolic values. This lesion topography is discussed in relation to the development of akinetic mutism in the present case and in comparison with recent reports on the topic. Considering a plausible pathophysiology, akinetic mutism appears to be based on a different structural neuropathology when compared with the locked-in syndrome and the vegetative state. It is suggested that akinetic mutism is regarded as a specific condition characterized by injury of the frontal neuronal systems which promote executive functions.- - - - - - - - - - ranking = 0.0004376418194729keywords = state (Clic here for more details about this article) |
10/22. Cyanide-induced akinetic rigid syndrome: clinical, MRI, FDG-PET, beta-CIT and HMPAO SPECT findings.A 35-year-old female ingested a lethal dose of potassium cyanide in a suicide attempt. She survived following antidote therapy and intensive care. Following artificial coma she presented with an agitative state for several days followed by akinetic mutism, buccofacial and ideomotoric aphasia. Severe rigid-akinetic syndrome, dysarthria, dysphagia and generalized dystonia developed weeks later. MRI revealed lesions in the caudate and lentiform nuclei, precentral cortex, and cerebellum. SPECT by [123-I] 2 beta-carbomethoxy-3-beta-(4-iodophenyl)-Tropan on two occasions revealed progressive loss of dopamine transporter suggestive of nigral neuronal apoptosis. Striatal and frontal hypometabolism and hypoperfusion were found by FDG-PET and HMPAO SPECT.- - - - - - - - - - ranking = 0.00021882090973645keywords = state (Clic here for more details about this article) |
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