A rare case of Holmes tremor in a worker with occupational carbon monoxide poisoning

Abstract

Parkinsonism and encephalopathy are frequently seen in patients who survive carbon monoxide (CO) poisoning. Neurological findings associated with CO poisoning can emerge immediately after cessation of exposure or following a brief period of pseudo‐recovery. When present, the tremor associated with CO poisoning is typical of the postural/intention type. Here, we report on a rare case of toxic encephalopathy with a dominant‐hand Holmes‐type tremor, characterized by resting, as well as postural and kinetic/intentional components, in a previously healthy 53‐year‐old man exposed to CO while actively engaged in the process of performing a physically demanding skilled labor task. The unique neuropathological and functional changes that give rise to Holmes‐type tremor and how this relates to the selective vulnerability of the inhibitory indirect pathway of the basal ganglia to glutamatergic excitotoxicity mediated by tissue hypoxia are discussed.

Evolving Concepts in Our Understanding and Treatment of Holmes Tremor, Over 100 Years in the Making

“…However, other studies report no significant correlations between lesion extent and the severity of associated neurologic manifestations [ 2 ]. As previously stated, this discrepancy extends to neuroimaging, with occasional dissociation between symptoms severity and degree of injury on MRI [ 12 13 14 15 ]. The latency from lesion to tremor onset is usually about two months and its generation likely relies on a combined involvement of both the dopaminergic nigrostriatal system and the cerebello-thalamo-cortical pathways.…”

“…Although these findings reinforce the importance of both the cerebello-thalamo-cortical and the dentato-rubro-olivary pathways in the development of HT, some cases lacked involvement of the nigrostriatal system [ 15 ]. Additional imaging studies support normal dopaminergic uptake in certain cases [ 12 13 14 15 ]. It should be noted however, that this occurrence is uncommon as evidenced by being reported primarily in individual case reports [ 3 14 15 ].…”

“…Most patients with HT have lesions in the thalamus or midbrain [ 10 11 ]. The mechanisms of injury to these pathways include ischemic or hemorrhagic vascular lesions as well as traumatic brain injury, although the development and progression of HT can be linked to demyelinating diseases, metastatic cancer, paraneoplastic disorders, environmental toxins, and viral infections [ 2 11 12 13 14 ] Specifically, ischemic or hemorrhagic vascular lesions represent approximately 48–55% of HT cases, while instances of traumatic brain injury make up approximately 17–20% of cases [ 2 10 ]. Some studies found that hemorrhage resulting from traumatic brain injury is a common factor in the development of HT [ 3 ].…”