holmes ' tremor , first described by gordon holmes in 1904 , is a rare condition characterized by symptomatic low frequency resting tremor , usually less than 4.5 hz , which is enhanced by posture , even more aggravated with action , disappears during sleep , and is generally unilateral.2 ) this tremor , also known as rubral , midbrain , or myorhythmia,6 ) typically involves the proximal regions of the limbs and occurs as a delayed manifestation of lesions involving the upper brain stem , areas adjacent to the red nucleus , substantia , and the nigrostriatal tract.9 ) hypertrophic olivary degeneration ( hod ) is a rare form of trans - synaptic neuronal degeneration representing the final result of alteration in the guillain - mollaret triangle ( denato - rubro - olivary pathway).3 ) holmes ' tremor is correlated with hod.9 ) brainstem insults leading to hod include infarction , infection , tumors , hemorrhage , and other demyelinating diseases . we report on a patient with brainstem hemorrhage whose magnetic resonance imaging ( mri ) showed evidence of bilateral hod , holmes ' tremor , and a palatal myoclonus . a 59-year - old woman who had hypertension was admitted due to sudden deterioration of a semicomatous mental state . neurological examination revealed pin point pupil , extension to pain , increased deep tendon reflexes , and positive for other pathologic reflexes . brain computed tomography ( ct ) scan on admission showed an acute hemorrhage in the pons ( fig . the patient received conservative management in the intensive care unit , and was eventually transferred to a rehabilitation facility at one month post - hemorrhage , where she continued to have quadriparesis , facial weakness , dysphasia requiring a feeding tube , and profound disequilibrium . her condition showed gradual improvement over several months ; she became alert , but still had significant diplopia , dysarthria , and paresthesia . seven months after the brainstem hemorrhage , the patient was reassessed because of deteriorated dysarthria and diplopia . she had low amplitude , irregular , coarse tremor of the right upper extremity at rest and posture that was further accentuated by action and did not occur during sleep . the tremor was flexion - extension oscillatory movement at the right upper extremity , most predominant distally , with a frequency of 2 - 4 hz . the patient also developed a bilateral palatal and irregular dystonic head tremor with aggravated horizontal diplopia . these lesions were hyperintense on a t2-weighted image and isointense on a t1-weighted image ( figs . as these symptoms progressed , her ability to perform activities of daily living worsened , including her ability to eat independently . she was treated sequentially with propranolol , clonazepam , trihexyphenidyl , and levitracetam , but her symptoms persisted . her medication was switched to gabapentin ( 900 mg ) for her sensory complaints and levodopa / carbidopa ( 250/25 mg ) for the tremor . initially , she was treated with small doses of levodopa / carbidopa but the dosage was increased progressively over the course of three months to reach a final dose of 250/25 mg three times per day . despite treatment with these drugs for three months , brain stem hemorrhage can cause development of holmes ' tremor.11 ) the movement disorder society has established three criteria for the diagnosis of holmes ' tremor ; ( 1 ) presence of both resting and intentional tremor , ( 2 ) a slow frequency , usually less than 4.5 hz , and ( 3 ) a variable delay ( usually months ) after occurrence of the lesion.2 ) holmes ' tremor is also known as a rubral tremor or midbrain tremor . the amplitude of the movement tends to be large and it can sometimes adopt a wing - beating appearance . in our case , the features were consistent with the reported criteria ; ( 1 ) low amplitude , irregular , coarse tremor at rest and posture , further accentuated by action and not occurring during sleep ; ( 2 ) predominantly unilateral ; ( 3 ) the tremor began seven months after the brainstem hemorrhage . as with cerebellar and symptomatic palatal tremor , rubral tremor arises from damage to the cerebellar and brainstem motor pathways and from dysregulation of motor control during movement . the pathogenesis of holmes ' tremor has been attributed to combined destruction of the pallidothalamic and cerebellothalamic pathways , with involvement of the rubro - olivo - cerebello - rubral loops and possibly the nigrostriatal system . this patient developed holmes ' tremor on the right upper extremity and brain mri showed evidence of hod seven months after the brain stem hemorrhage ; palatal tremor was also observed . symptomatic palatal tremor is a pathologically and anatomically well - defined disorder that commonly appears after disruption of the guillain - mollaret triangle ( also known as the dentato - rubro - olivary pathway).3 ) palatal tremor is correlated with hod . an unusual form of transneuronal degeneration is the enlargement , rather than atrophy , of the affected inferior olivary nuclei.13 ) hod is predominantly unilateral ; however , rare bilateral cases have been reported.5)7 ) midline lesion or lesions in the superior cerebellar peduncle can result in bilateral hod ( interrupting decussation of the dentato - rubro - olivary pathway).1 ) central nervous system degeneration leads to atrophy characterized by neuronal loss and proliferation of glial elements . pathological findings of hod are cytoplasmic vacuolar degeneration , neuronal enlargement , gliosis , and glial hypertrophy . these changes lead to macroscopic enlargement of the olive with corresponding non - enhancing focus of t2 hyperintensity on mri , which is characteristic of hod . the differential diagnosis for a t2 hyperintense lesion in the olivary region includes infarct , neoplasm , demyelinating process , and infection . however , the lack of enhancement excludes the majority of neoplastic and infectious entities and enlargement of the olive would be atypical in the setting of infarction or chronic demyelination . the most important clue is its association with the inciting lesion of the contralateral cerebellum or ipsilateral brain stem . the delayed - onset between insult and tremor following a structural lesion of the brain is well described but poorly understood . the delay between brain stem insult and tremor is unpredictable but usually occurs at around four weeks to two years . this may be related to transneuronal plastic changes occurring at the neuronal level.9)10 ) in review of the literature , we found a few case reports of holmes ' tremor secondary to brainstem hemorrhage that responded to levodopa.8)12 ) however , the drug therapy is usually unsuccessful . because the success rate of medical treatment is low , some patients are referred for surgery . the commonly chosen target for deep brain stimulation ( dbs ) is the ventrolateral nucleus of the thalamus . thalamic dbs has therefore often been applied for the surgical treatment of holmes ' tremor.4 ) treatment of holmes ' tremor should be individualized . surgery may be considered for patients who do not respond to the usual medical treatment . hod is associated with delayed neurological deterioration including holmes ' tremor after brain stem hemorrhage . surgery may be considered for patients who do not respond to the usual medical treatment .
holmes ' tremor is a condition characterized by a mixture of postural , rest , and action tremors due to midbrain lesions in the vicinity of the red nucleus . 
 hypertrophic olivary degeneration ( hod ) is a rare type of neuronal degeneration involving the dento - rubro - olivary pathway and may present clinically as holmes tremor . 
 we report on a 59-year - old female patient who developed holmes tremor in association with bilateral hod , following brain stem hemorrhage .