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Archivio Di Psicologia, Neurologia E... 1958
Topics: Akinetic Mutism; Behavior; Biomedical Research; Hemorrhage; Humans; Speech Disorders
PubMed: 13522433
DOI: No ID Found -
Bone Marrow Transplantation Jan 2013
Topics: Akinetic Mutism; Drug Monitoring; Drug Therapy, Combination; Female; Graft vs Host Disease; Humans; Immunosuppressive Agents; Leukemia, Myeloid, Acute; Middle Aged; Neurotoxicity Syndromes; Nuclear Family; Stem Cell Transplantation; Tacrolimus; Treatment Outcome
PubMed: 22705799
DOI: 10.1038/bmt.2012.110 -
Neurotoxicology Dec 2010A 49-year-old woman developed a catatonic mute state a few weeks after methadone overdose. Clinical, radiological and histological findings were consistent with toxic...
A 49-year-old woman developed a catatonic mute state a few weeks after methadone overdose. Clinical, radiological and histological findings were consistent with toxic spongiform leukoencephalopathy, which adds a potentially deadly side-effect to a generally considered safe substitution for heroin.
Topics: Akinetic Mutism; Catatonia; Drug Overdose; Female; Humans; Leukoencephalopathies; Methadone; Time Factors
PubMed: 20688102
DOI: 10.1016/j.neuro.2010.07.007 -
European Archives of Psychiatry and... 1988The clinical symptoms and neuropathological findings of three patients suffering from akinetic mutism were summarized. The patients showed almost absolute mutism and...
The clinical symptoms and neuropathological findings of three patients suffering from akinetic mutism were summarized. The patients showed almost absolute mutism and immobility and were unable to communicate in any way. The neurological signs varied from case to case. The pathological features common to all of the cases were bilateral lesions of the rostral part of the anterior cingulate gyri which overlapped onto the neighboring supplementary motor area, while differing as regards other damage. With the help of more recent neurobiochemical findings we tried to analyze the pathomechanism of akinetic mutism on the basis of the structures damaged. There seems to be an anatomic correspondence between the mesolimbocortical dopaminergic system and the circumscribed bilateral lesions of the medial prefrontal cortex. The study suggests that damage of the mesolimbocortical dopaminergic terminal fields in the anteromedial frontal cortex is essential for this specific type of akinetic mutism.
Topics: Aged; Akinetic Mutism; Brain Damage, Chronic; Brain Neoplasms; Cerebral Hemorrhage; Cerebral Infarction; Female; Glioblastoma; Gyrus Cinguli; Humans; Male; Middle Aged; Receptors, Dopamine
PubMed: 2849547
DOI: 10.1007/BF00449910 -
Psychological Medicine Feb 1971
Topics: Acute Disease; Adult; Akinetic Mutism; Carbon Monoxide Poisoning; Electroencephalography; Hospitalization; Humans; Male; Oxygen Inhalation Therapy; Patient Readmission; Personality Disorders; Phenytoin; Prognosis
PubMed: 5148768
DOI: 10.1017/s0033291700000106 -
Prion Dec 2021Methionine/methionine type 1 (MM1-type) sporadic Creutzfeldt-Jakob disease (sCJD), known as the 'classic type,' shows typical clinicopathological sCJD findings. In...
Methionine/methionine type 1 (MM1-type) sporadic Creutzfeldt-Jakob disease (sCJD), known as the 'classic type,' shows typical clinicopathological sCJD findings. In general, patients reach an akinetic mutism state within a few months of disease onset and die soon after if supportive therapies are not administered. Here, we describe remarkable neuropathologic observations of MM1-type sCJD in a 48-year-old, Japanese man with an unusually prolonged akinetic mutism state. In the early disease stages, the patient exhibited abnormal behaviour with gait disturbance and rapidly progressive cognitive dysfunction. Diffusion-weighted magnetic resonance imaging revealed extensive cerebral cortical hyperintensity. Prion protein (PrP) gene analysis revealed no mutations, and the polymorphic codon 129 exhibited methionine homozygosity. Although the patient remained stable with tube feeding for more than 2 years after reaching the akinetic mutism state, he died because of central respiratory failure 30 months after disease onset. Neuropathologic investigation showed extensive devastating lesions, such as status spongiosus, and typical spongiform changes could no longer be observed in the cerebral neocortex. Conspicuous pyramidal tract degeneration was observed. However, the regions commonly preserved in MM1-type sCJD pathology were still relatively preserved. Immunostaining revealed extensive diffuse synaptic-type PrP deposition in the grey matter. The pathological findings suggested that sCJD is a neurodegenerative disease that shows system degeneration; there are primary and secondary degenerative regions and distinct preserved regions, even in cases with prolonged disease duration. In addition, it is considered that there is a limited survival period for MM1-type sCJD, even if active symptomatic treatment is provided.
Topics: Akinetic Mutism; Creutzfeldt-Jakob Syndrome; Humans; Male; Methionine; Middle Aged; Neurodegenerative Diseases; Prion Proteins
PubMed: 33472525
DOI: 10.1080/19336896.2020.1868931 -
Pharmacotherapy Apr 1999A 76-year-old man developed akinetic mutism after 3 days of receiving low-dosage baclofen. Electroencephalography showed a diffusely slow background with intermittent...
A 76-year-old man developed akinetic mutism after 3 days of receiving low-dosage baclofen. Electroencephalography showed a diffusely slow background with intermittent generalized sharp wave discharges. The condition resolved after discontinuing baclofen. To our knowledge, this is the first reported case of baclofen-induced akinetic mutism in a patient with normal renal function. The pathophysiology of this condition is unknown, but it may result from selective binding of the drug to the gamma-aminobutyric acid-B receptors located in the frontal lobes or thalamic nuclei, interrupting the thalamocortical limbic pathways.
Topics: Aged; Akinetic Mutism; Baclofen; GABA Agonists; Humans; Male
PubMed: 10212020
DOI: 10.1592/phco.19.6.468.31053 -
Schizophrenia Research Jan 2024Catatonia occurs secondary to both primary psychiatric and neuromedical etiologies. Emerging evidence suggests possible linkages between causes of catatonia and...
Catatonia occurs secondary to both primary psychiatric and neuromedical etiologies. Emerging evidence suggests possible linkages between causes of catatonia and neuroinflammation. These include obvious infectious and inflammatory etiologies, common neuromedical illnesses such as delirium, and psychiatric entities such as depression and autism-spectrum disorders. Symptoms of sickness behavior, thought to be a downstream effect of the cytokine response, are common in many of these etiologies and overlap significantly with symptoms of catatonia. Furthermore, there are syndromes that overlap with catatonia that some would consider variants, including neuroleptic malignant syndrome (NMS) and akinetic mutism, which may also have neuroinflammatory underpinnings. Low serum iron, a common finding in NMS and malignant catatonia, may be caused by the acute phase response. Cellular hits involving either pathogen-associated molecular patterns (PAMP) danger signals or the damage-associated molecular patterns (DAMP) danger signals of severe psychosocial stress may set the stage for a common pathway immunoactivation state that could lower the threshold for a catatonic state in susceptible individuals. Immunoactivation leading to dysfunction in the anterior cingulate cortex (ACC)/mid-cingulate cortex (MCC)/medial prefrontal cortex (mPFC)/paralimbic cortico-striato-thalamo-cortical (CSTC) circuit, involved in motivation and movement, may be particularly important in generating the motor and behavioral symptoms of catatonia.
Topics: Humans; Catatonia; Neuroleptic Malignant Syndrome
PubMed: 36966063
DOI: 10.1016/j.schres.2023.03.013 -
The European Journal of Neuroscience Mar 2024The clinical assessment of patients with disorders of consciousness (DoC) relies on the observation of behavioural responses to standardised sensory stimulation....
The clinical assessment of patients with disorders of consciousness (DoC) relies on the observation of behavioural responses to standardised sensory stimulation. However, several medical comorbidities may directly impair the production of reproducible and appropriate responses, thus reducing the sensitivity of behaviour-based diagnoses. One such comorbidity is akinetic mutism (AM), a rare neurological syndrome characterised by the inability to initiate volitional motor responses, sometimes associated with clinical presentations that overlap with those of DoC. In this paper, we describe the case of a patient with large bilateral mesial frontal lesions, showing prolonged behavioural unresponsiveness and severe disorganisation of electroencephalographic (EEG) background, compatible with a vegetative state/unresponsive wakefulness syndrome (VS/UWS). By applying an unprecedented multimodal battery of advanced imaging and electrophysiology-based techniques (AIE) encompassing spontaneous EEG, evoked potentials, event-related potentials, transcranial magnetic stimulation combined with EEG and structural and functional MRI, we provide the following: (i) a demonstration of the preservation of consciousness despite unresponsiveness in the context of AM, (ii) a plausible neurophysiological explanation for behavioural unresponsiveness and its subsequent recovery during rehabilitation stay and (iii) novel insights into the relationships between DoC, AM and parkinsonism. The present case offers proof-of-principle evidence supporting the clinical utility of a multimodal hierarchical workflow that combines AIEs to detect covert signs of consciousness in unresponsive patients.
Topics: Humans; Akinetic Mutism; Unconsciousness; Consciousness; Electroencephalography; Electric Stimulation Therapy
PubMed: 37077023
DOI: 10.1111/ejn.15994 -
Journal of the Neurological Sciences May 2020
Topics: Akinetic Mutism; Cerebral Cortex; Creutzfeldt-Jakob Syndrome; Humans
PubMed: 32114028
DOI: 10.1016/j.jns.2020.116759