On the nature of brain stem disorders in severe head injured patients

Minderhoud, J.M.; Vanwoerkom, Tcam; Vanweerden, Tw

doi:10.1007/bf01405860

Cited by 14 publications

(3 citation statements)

References 17 publications

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“…Specific pathways discussed in literature include interconnections that originate within the midbrain, spinal cord, and frontal lobe. Using this model, damage to any of these interconnections could hypothetically result in abulia (36,37).…”

Section: Discussionmentioning

confidence: 44%

Treatment of Abulia with Carbidopa/Levodopa

Drubach¹,

Zeilig

Pérez

et al. 1995

Neurorehabilitation and Neural Repair

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Abulia is a clinical syndrome manifested by lack of spontaneity of action and speech, deficiency in initiation, apathy, inertia, mental and motor slowness, reduction in excursion of motion, poor attention, and easy distractibility. Abulia has been conceptualized as laying in a continuum of motivational and emotional deficit in which apathy is at one extreme and akinetic mutism at the other, more severe extreme. Lesions in the frontal lobes have been most often implicated in the causality of abulia, but other areas of involvement have also been described. Some authors have reported the beneficial effect of dopaminergic agents in the treatment of abulia and other related disorders. We report on four patients with various disorders of the CNS and abulic symptoms who had a beneficial response to administration of a carbidopa/levodopa (Sinemet) compound many months after the CNS insult responsible for the symptoms. We hypothesize that levodopa may be beneficial in the treatment of abulia by increasing the availability of dopamine to the prefrontal cortex or related areas in the brain.

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Section: Discussionmentioning

confidence: 44%

Treatment of Abulia with Carbidopa/Levodopa

Drubach¹,

Zeilig

Pérez

et al. 1995

Neurorehabilitation and Neural Repair

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“…Only three studies have investigated the use of vestibular stimulation in patients with severe brain injuries. Two early studies demonstrated a correlation between electrooculographic recordings after CVS and the state of consciousness, but the duration of this effect was unclear [ 206 , 207 ]. The third study showed time-locked behavioral improvements in two patients in a chronic MCS using a crossover design over 16–18 weeks of CVS and sham stimulation [ 208 ].…”

Section: Sensory Therapiesmentioning

confidence: 99%

Therapies to Restore Consciousness in Patients with Severe Brain Injuries: A Gap Analysis and Future Directions

et al. 2021

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Background/Objective For patients with disorders of consciousness (DoC) and their families, the search for new therapies has been a source of hope and frustration. Almost all clinical trials in patients with DoC have been limited by small sample sizes, lack of placebo groups, and use of heterogeneous outcome measures. As a result, few therapies have strong evidence to support their use; amantadine is the only therapy recommended by current clinical guidelines, specifically for patients with DoC caused by severe traumatic brain injury. To foster and advance development of consciousness-promoting therapies for patients with DoC, the Curing Coma Campaign convened a Coma Science Work Group to perform a gap analysis. Methods We consider five classes of therapies: (1) pharmacologic; (2) electromagnetic; (3) mechanical; (4) sensory; and (5) regenerative. For each class of therapy, we summarize the state of the science, identify gaps in knowledge, and suggest future directions for therapy development. Results Knowledge gaps in all five therapeutic classes can be attributed to the lack of: (1) a unifying conceptual framework for evaluating therapeutic mechanisms of action; (2) large-scale randomized controlled trials; and (3) pharmacodynamic biomarkers that measure subclinical therapeutic effects in early-phase trials. To address these gaps, we propose a precision medicine approach in which clinical trials selectively enroll patients based upon their physiological receptivity to targeted therapies, and therapeutic effects are measured by complementary behavioral, neuroimaging, and electrophysiologic endpoints. Conclusions This personalized approach can be realized through rigorous clinical trial design and international collaboration, both of which will be essential for advancing the development of new therapies and ultimately improving the lives of patients with DoC.

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“…Etiologies of AM ranged from infarction, tumors, ruptured aneurysnia, arteriovenous malformation, third ventricular cyst, hydrocephalus, encephalitis, meningitis and trauma (21). N-B disease is a rare cause of AM.…”

mentioning

confidence: 99%

Mutism developing after bilateral thalamo-capsular lesions by neuro-Behçet disease

Park-Matsumoto¹,

Ogawa²,

Tazawa³

et al. 1995

Acta Neurologica Scandinavica

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We described a 44-year old right-handed man showing mutism, left hemiplegia and pseudobulbar palsy after CT and MRI documented bilateral thalamo-capsular lesions by neuro-Behçet disease. Single photon emission tomography (SPECT) and Xenon CT revealed hypoperfusion of the bilateral frontal lobes. The pathophysiological mechanism of mutism was discussed and we postulate that mutism might occur as the result of frontal lobe dysfunction due to the disconnection of thalamocortical fiber from thalamus to frontal cortex and that it could be interpreted as an incomplete form of akinetic mutism.

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On the nature of brain stem disorders in severe head injured patients

Cited by 14 publications

References 17 publications

Treatment of Abulia with Carbidopa/Levodopa

Treatment of Abulia with Carbidopa/Levodopa

Therapies to Restore Consciousness in Patients with Severe Brain Injuries: A Gap Analysis and Future Directions

Mutism developing after bilateral thalamo-capsular lesions by neuro-Behçet disease

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