Holmes tremor in association with bilateral hypertrophic olivary degeneration and palatal tremor: chronological considerations. Case report

Rieder, Carlos Roberto de Mello; Rebouças, Ricardo Gurgel; Ferreira, Marcelo Paglioli

doi:10.1590/s0004-282x2003000300028

Cited by 38 publications

(31 citation statements)

References 13 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Head trauma accounted for almost 20% of the cases in previous publications, 1,[3][4][5]7,8,,e1-e52 while we found 17.24% traumatic cases in our series (table e-1).…”

Section: Opportunistic Infection In Aidssupporting

confidence: 50%

“…4,10,40,e2,e5,e7,e8,e13,e15,e18,e23, e31,e34,e35,e37,e50 In 3 patients from our series, thalamotomy of VIM showed excellent improvement. In some cases, it has been necessary to make a combined DBS of VIM and subthalamic nucleus to effectively control HT.…”

Section: Opportunistic Infection In Aidsmentioning

confidence: 66%

“…This tremor is also known as rubral, mesencephalic, or thalamic tremor, but these terms are no longer used because typical cases have been described with lesions located in other areas, and red nucleus experimental lesions fail to induce persistent tremor. [2][3][4][5] The current definition of HT is derived from the Consensus Statement of the Movement Disorder Society on Tremor from 1998. 6 It is described as a rest and intention tremor with sometimes irregular amplitude.…”

mentioning

confidence: 99%

See 2 more Smart Citations

Holmes tremor

et al. 2016

View full text Add to dashboard Cite

Objective: To describe the clinical features, etiology, findings from neuroimaging, and treatment results in a series of 29 patients with Holmes tremor (HT).Methods: A retrospective study was performed based on review of medical records and videos of patients with HT diagnosis.Results: A total of 16 women and 13 men were included. The mean age at the moment of CNS insult was 33.9 6 20.1 years (range 8-76 years). The most common causes were vascular (48.3%), ischemic, or hemorrhagic. Traumatic brain injury only represented 17.24%; other causes represented 34.5%. The median latency from lesion to tremor onset was 2 months (range 7 days-228 months). The most common symptoms/signs associated with HT were hemiparesis (62%), ataxia (51.7%), hypoesthesia (27.58%), dystonia (24.1%), cranial nerve involvement (24.1%), and dysarthria (24.1%). Other symptoms/signs were vertical gaze disorders (6.8%), bradykinesia/rigidity (6.8%), myoclonus (3.4%), and seizures (3.4%). Most of the patients had lesions involving more than one area. MRI showed lesions in thalamus or midbrain or cerebellum in 82.7% of the patients. Levodopa treatment was effective in 13 out of 24 treated patients (54.16%) and in 3 patients unilateral thalamotomy provided excellent results. Conclusions:The most common causes of HT in our series were vascular lesions. The most common lesion topography was mesencephalic, thalamic, or both. Treatment with levodopa and thalamic stereotactic lesional surgery seems to be effective.

show abstract

“…Head trauma accounted for almost 20% of the cases in previous publications, 1,[3][4][5]7,8,,e1-e52 while we found 17.24% traumatic cases in our series (table e-1).…”

Section: Opportunistic Infection In Aidssupporting

confidence: 50%

Section: Opportunistic Infection In Aidsmentioning

confidence: 66%

mentioning

confidence: 99%

See 1 more Smart Citation

Holmes tremor

et al. 2016

View full text Add to dashboard Cite

show abstract

“…1 It is also known as midbrain or rubral tremor; however, these terms should not be used because many typical cases have been reported with lesions in other locations. 2,3 Moreover, it has been found that lesions in the red nucleus in experimental models fail to induce persistent tremor. 2,4 This type of tremor occurs as a delayed manifestation of lesions involving the cerebellifugal fibers in the upper region of the brainstem, areas adjacent to the red nucleus, substantia nigra, and the nigrostriatal pathway.…”

mentioning

confidence: 99%

“…2,4 This type of tremor occurs as a delayed manifestation of lesions involving the cerebellifugal fibers in the upper region of the brainstem, areas adjacent to the red nucleus, substantia nigra, and the nigrostriatal pathway. 1,3 Lesions associated with Holmes tremor may have different etiologies, including ischemic or hemorrhagic cerebrovascular disorders, bleeding secondary to vascular malformations, head and brain trauma, tumors, demyelination, and infections. 5 We report 2 cases of Holmes tremor secondary to midbrain hemorrhagic lesions otherwise unresponsive to medical treatment, which responded markedly to levodopa.…”

mentioning

confidence: 99%

Holmes Tremor Secondary to Brainstem Hemorrhage Responsive to Levodopa

Raina¹,

Vélez²,

Pardal³

et al. 2007

Clinical Neuropharmacology

View full text Add to dashboard Cite

We report 2 patients who presented a brainstem hemorrhage and who, after 1 and 6 months, respectively, developed a 4-Hz postural and resting tremor consistent with Holmes tremor, which severely interfered with the activities of daily living. In both cases, levodopa dramatically improved the tremor. Pharmacological treatment of this condition is usually disappointing, and surgical procedures are commonly required for severe cases. Our patients, together with 13 others gleaned from the literature, suggest that in cases of Holmes tremor secondary to brainstem hemorrhage, levodopa can be a useful treatment, and it should be tested before considering invasive therapies.

show abstract

Unusual Clinical Manifestation Associated with Hypertrophic Olivary Degeneration

Fattouch

Conte

Colonnese

et al. 2014

Movement Disord Clin Pract

View full text Add to dashboard Cite

Hypertrophic olivary degeneration (HOD) is a rare abnormality that is caused by a lesion in the Guillain-Mollaret triangle in the brainstem. 1,2 HOD usually occurs uni-and ipsilaterally to the lesion if the lesion is in the brainstem or contralaterally to the lesion if the lesion is in the cerebellum, as has been shown by MRI. The Guillain-Mollaret triangle is composed of the contralateral dentate nucleus, the ipsilateral red nucleus, and the ipsilateral inferior olivary nucleus (ION). The ION is a highly developed complex that is the main source of climbing fibers to the cerebellum. These fibers have powerful excitatory synapses on Purkinje cell dendrites. The inferior olive tends to possess a slow, rhythmic, spontaneous activity. HOD usually manifests itself with palatal myoclonus. 3,4 The causes of HOD include trauma, inflammation, tumor, degenerative disease, and surgical manipulation. We describe a 52-year-old woman who developed an unusual clinical presentation associated with HOD. Case ReportThe patient's history started 4 months before she was admitted to our hospital, when she complained of subjective balance disturbances. A neurological examination performed in another hospital had been considered normal. A brain MRI revealed cerebral (right parieto-occipital region and right and left temporal lobe at the subcortical level) and cerebellar (vermis, right cerebellar hemisphere, and the left cerebellar peduncle) metastases. MRI also showed a slightly increased T2 signal intensity in the right olivary nucleus. A total body CT detected lung cancer. She underwent resection of the cerebellar metastasis. After surgery, she presented gait ataxia and, approximately 20 days later, she progressively developed headache, dysarthria, an inability to walk as a result of ataxia, upper-limb plegia, and involuntary head movements. No palatal myoclonus was observed. A ventricular derivation was performed, though to no beneficial effect. Upon admission to our department (approximately 40 days after surgery), she was in a stuporous state with bilateral upper-limb plegia, as well as asynchronous involuntary head and jaw movements characterized by latero-lateral oscillations of the head and jaw (see Video 1). The right eye was directed toward the right, whereas the left eye was in the primary position. Gaze could be oriented toward the verbal stimulus. The patient did not have nystagmus. Pursuit movements could not be assessed. The involuntary movements persisted for most of the day, increasing in intensity after verbal and tactile stimulation, but disappeared during sleep. Although we did not perform electromyography, a video recording allowed us to estimate that the frequency of the latero-lateral oscillations was in the range of 2 to 3 Hz. EEG excluded epileptic abnormalities and documented regular physiological sleep features. Meningeal carcinomatosis and paraneoplastic syndrome were ruled out by the absence of neoplastic cells and cerebellar autoantibodies in the liquor. Brain MRI revealed increased T2 signal intensity in...

show abstract

Holmes tremor in association with bilateral hypertrophic olivary degeneration and palatal tremor: chronological considerations. Case report

Cited by 38 publications

References 13 publications

Holmes tremor

Holmes tremor

Holmes Tremor Secondary to Brainstem Hemorrhage Responsive to Levodopa

Unusual Clinical Manifestation Associated with Hypertrophic Olivary Degeneration

Contact Info

Product

Resources

About