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HOLMESTREMOR
AdeWijaya, MD
February 2018
Outline:
■ Introduction
■ Pathophysiology
■ Etiology
■ Associated clinical manifestation
■ Site of lesions
■ Treatment
■ Summary
Introduction
■ Holmes tremor (HT) was first described in 1904 by Gordon Holmes as a 3–4 Hz flexor
extension oscillation, present at rest and exacerbated with posture and additionally
intensified with action.
■ This tremor is also known as rubral, mesencephalic, or thalamic tremor
■ A rest and intention tremor with sometimes irregular amplitude
■ Tremor commonly develops between 1 and 24 months after a CNS insult.This delayed
onset might be due to neuronal plastic changes
Raina, G. B., Cersosimo, M. G., Folgar, S. S., Giugni, J. C., Calandra, C., Paviolo, J. P., ... & Pellene, L. A. (2016). Holmes tremor Clinical description, lesion localization, and treatment in a series of 29
cases. Neurology, 86(10), 931-938.
Pathophysiology
It is assumed that a double lesion is required to develop HT, including:
■ The dopaminergic nigrostriatal system
■ The cerebello-thalamo-cortical pathways
■ The dentate-rubro-olivary pathways (Guillain-Mollaret triangle)
Raina, G. B., Cersosimo, M. G., Folgar, S. S., Giugni, J. C., Calandra, C., Paviolo, J. P., ... & Pellene, L. A. (2016). Holmes tremor Clinical description, lesion localization, and treatment in a series of 29
cases. Neurology, 86(10), 931-938.
Etiology
Raina, G. B., Cersosimo, M. G., Folgar, S. S., Giugni, J. C., Calandra,
C., Paviolo, J. P., ... & Pellene, L. A. (2016). Holmes tremor Clinical
description, lesion localization, and treatment in a series of 29
cases. Neurology, 86(10), 931-938.
Associated Clinical Manifestation
■ Hemiparesis
■ Ataxia
■ Hypesthesia
■ Dystonia
■ Dysartria
■ Cranial nerve palsies
■ Vertical gaze alteration
■ Bradykinesia / rigidity
■ Myoclonus
■ Psychiatric disorders
■ seizure
Raina, G. B., Cersosimo, M. G., Folgar, S. S., Giugni, J. C., Calandra, C., Paviolo, J. P., ... & Pellene, L. A. (2016). Holmes tremor Clinical description, lesion localization, and treatment in a series of 29
cases. Neurology, 86(10), 931-938.
Site of Lesions
■ Thalamus
■ Midbrain
■ Pons
■ Medulla oblongata
■ Cerebellum
■ Others
Raina, G. B., Cersosimo, M. G., Folgar, S. S., Giugni, J. C., Calandra, C., Paviolo, J. P., ... & Pellene, L. A. (2016). Holmes tremor Clinical description, lesion localization, and treatment in a series of 29
cases. Neurology, 86(10), 931-938.
Treatment
■ LEVODOPA
■ Botox injection
■ Dopaminergic agonists, anticholinergic drugs, clonazepam, levetiracetam, and
carbamazepine
■ DBS or thalamotomy or phallidotomy (ventral intermediate nucleus / GPi)
Raina, G. B., Cersosimo, M. G., Folgar, S. S., Giugni, J. C., Calandra, C., Paviolo, J. P., ... & Pellene, L. A. (2016). Holmes tremor Clinical description, lesion localization, and treatment in a series of 29
cases. Neurology, 86(10), 931-938.
Summary
■ HT is a 3–4 Hz flexor extension oscillation, present at rest and exacerbated with
posture and additionally intensified with action.
■ The most common etiology is vascular.
■ The most common site of lesions are mesencephalon and thalamus.
■ The most common associated symptoms are hemiparesis and ataxia.
■ The most effective treatment is functional surgery
■ Levodopa may be effective.
Holmes Tremor  0218

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Holmes Tremor 0218

  • 2. Outline: ■ Introduction ■ Pathophysiology ■ Etiology ■ Associated clinical manifestation ■ Site of lesions ■ Treatment ■ Summary
  • 3. Introduction ■ Holmes tremor (HT) was first described in 1904 by Gordon Holmes as a 3–4 Hz flexor extension oscillation, present at rest and exacerbated with posture and additionally intensified with action. ■ This tremor is also known as rubral, mesencephalic, or thalamic tremor ■ A rest and intention tremor with sometimes irregular amplitude ■ Tremor commonly develops between 1 and 24 months after a CNS insult.This delayed onset might be due to neuronal plastic changes Raina, G. B., Cersosimo, M. G., Folgar, S. S., Giugni, J. C., Calandra, C., Paviolo, J. P., ... & Pellene, L. A. (2016). Holmes tremor Clinical description, lesion localization, and treatment in a series of 29 cases. Neurology, 86(10), 931-938.
  • 4. Pathophysiology It is assumed that a double lesion is required to develop HT, including: ■ The dopaminergic nigrostriatal system ■ The cerebello-thalamo-cortical pathways ■ The dentate-rubro-olivary pathways (Guillain-Mollaret triangle) Raina, G. B., Cersosimo, M. G., Folgar, S. S., Giugni, J. C., Calandra, C., Paviolo, J. P., ... & Pellene, L. A. (2016). Holmes tremor Clinical description, lesion localization, and treatment in a series of 29 cases. Neurology, 86(10), 931-938.
  • 5. Etiology Raina, G. B., Cersosimo, M. G., Folgar, S. S., Giugni, J. C., Calandra, C., Paviolo, J. P., ... & Pellene, L. A. (2016). Holmes tremor Clinical description, lesion localization, and treatment in a series of 29 cases. Neurology, 86(10), 931-938.
  • 6. Associated Clinical Manifestation ■ Hemiparesis ■ Ataxia ■ Hypesthesia ■ Dystonia ■ Dysartria ■ Cranial nerve palsies ■ Vertical gaze alteration ■ Bradykinesia / rigidity ■ Myoclonus ■ Psychiatric disorders ■ seizure Raina, G. B., Cersosimo, M. G., Folgar, S. S., Giugni, J. C., Calandra, C., Paviolo, J. P., ... & Pellene, L. A. (2016). Holmes tremor Clinical description, lesion localization, and treatment in a series of 29 cases. Neurology, 86(10), 931-938.
  • 7. Site of Lesions ■ Thalamus ■ Midbrain ■ Pons ■ Medulla oblongata ■ Cerebellum ■ Others Raina, G. B., Cersosimo, M. G., Folgar, S. S., Giugni, J. C., Calandra, C., Paviolo, J. P., ... & Pellene, L. A. (2016). Holmes tremor Clinical description, lesion localization, and treatment in a series of 29 cases. Neurology, 86(10), 931-938.
  • 8. Treatment ■ LEVODOPA ■ Botox injection ■ Dopaminergic agonists, anticholinergic drugs, clonazepam, levetiracetam, and carbamazepine ■ DBS or thalamotomy or phallidotomy (ventral intermediate nucleus / GPi) Raina, G. B., Cersosimo, M. G., Folgar, S. S., Giugni, J. C., Calandra, C., Paviolo, J. P., ... & Pellene, L. A. (2016). Holmes tremor Clinical description, lesion localization, and treatment in a series of 29 cases. Neurology, 86(10), 931-938.
  • 9. Summary ■ HT is a 3–4 Hz flexor extension oscillation, present at rest and exacerbated with posture and additionally intensified with action. ■ The most common etiology is vascular. ■ The most common site of lesions are mesencephalon and thalamus. ■ The most common associated symptoms are hemiparesis and ataxia. ■ The most effective treatment is functional surgery ■ Levodopa may be effective.