Long term follow up of a hemimasticatory spasm

Esteban, Ángel; Traba, A.; Prieto, J.; Grandas, Francisco

doi:10.1034/j.1600-0404.2002.00119.x

Cited by 27 publications

(29 citation statements)

References 21 publications

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“…Similar to our patient, most previously reported cases of HMS had normal blink reflex studies, indicating that ophthalmic branch (V1) of the trigeminal nerve was not affected. 2,4,5,8,9 Our patient was different in that he had clear sensory deficits that are also attributed to trigeminal nerve lesions-specifically the decreased facial sensation and corneal reflex (figure, B).…”

Section: -3mentioning

confidence: 72%

Clinical Reasoning: A 57-year-old man with jaw spasms

et al. 2013

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A 57-year-old man presented with spasms of his left jaw. Two years prior, he had developed left-sided facial numbness followed by development of left-sided shock-like pain and then involuntary and repetitive movements of the jaw-closing muscles. Jaw muscle contractions were episodic, interfered with chewing and talking, and led to frequent tongue biting. Individual spasms varied from seconds to minutes and he reported that function in between episodes was normal, although his wife felt he spoke with reduced mouth opening. He sometimes awoke with a bloody tongue, suggesting that contractions occurred during waking and sleep. He had no history of premonitory sensation or relief associated with the spasms. He reported no difficulty swallowing.Neurologic examination demonstrated decreased sensation in all 3 trigeminal divisions on the left and a reduced corneal reflex on the left. Masseter bulk, tone, and strength were normal bilaterally. Contractions were noted in the jaw-closing muscles. Mouth opening was limited during speech. There was no facial weakness. There was no palatal tremor. Head rotation, shoulder shrugging, and tongue movements were normal. With the exception of mild-to-moderate distal sensory deficit, the remainder of the neurologic examination was unremarkable.Questions for consideration: This patient's examination revealed 2 localizing abnormalities: decreased left facial sensation with diminished corneal reflex and frequent contractions of the left jaw muscles. Both findings localize to the trigeminal nerve. The sensory fibers of the trigeminal nerve originate at the trigeminal nucleus in the pons and the motor fibers of the trigeminal nerve originate in the pons in an area close to, but not in, the trigeminal nucleus. Sensory fibers project from the trigeminal nucleus to the trigeminal ganglion, at which point they split into 3 branch distributions: ophthalmic (V1), maxillary (V2), and mandibular (V3). Motor fibers project from the pons, decussate, track adjacent to the trigeminal nucleus, and eventually exit the cranium adjacent to V3 through the foramen ovale. From the foramen ovale, motor fibers separate from sensory fibers and radiate to the masseter and other jaw-moving muscles.The sensory and motor branches of this patient's nerve were both affected. We therefore infer that an intracranial lesion of the trigeminal nerve must be causing the patient's difficulties. Possible etiologies of the lesion include vascular, infectious, autoimmune, trauma, or a mass. The slow onset of this patient's difficulties decreases the likelihood of vascular lesions and there was no history of trauma. A lesion isolated to the trigeminal nerve would be an unusual presentation of an infectious or autoimmune etiology such as multiple sclerosis, Devic disease, or Listeria, and the patient had no current or past symptoms consistent with these illnesses. Considering these factors, the most likely etiology of this patient's isolated trigeminal nerve problem is a central tumor or mass. EMG recordings demonstrated fasci...

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Section: -3mentioning

confidence: 72%

Clinical Reasoning: A 57-year-old man with jaw spasms

et al. 2013

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“…Oral drugs, such as carbamazepine, phenytoin, and clonazepam, may be useful. BTX has become the preferred treatment because of excellent outcomes . On reviewing literature, we could find 18 cases of HMS with excellent response to BTX.…”

Section: Discussionmentioning

confidence: 99%

Hemi Masticatory Spasm: Series of 7 Cases and Review of Literature

Radhakrishnan

Goyal

Shukla

et al. 2019

Movement Disord Clin Pract

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Background Hemi masticatory spasm (HMS) is a rare movement disorder affecting muscles of mastication attributed to dysfunction of motor branch of trigeminal nerve and is characterized by painful spasm of masticatory muscles. Microvascular compression leading to focal demyelination of motor branch of trigeminal nerve is the most speculated on mechanism of HMS. Treatment options range from medical to surgical approaches, but botulinm toxin (BTX) has now become the preferred treatment. Cases We report a retrospective review of 7 cases of HMS, supported by electrophysiological and clinical findings. All the cases had excellent response to BTX therapy. Discussion and Conclusion In this article, we highlight the delay in diagnosis of HMS attributed to rarity, long course of illness, association with hemiatrophy, “Lichen Sclerosus et Atrophicus,” and scleroderma/morphea. Considering the favorable outcome to BTXs, surgical treatment can be avoided or delayed in majority except secondary cases.

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“…On the other hand, Cruccu et al [26] studied the masseter inhibitory reflex in 15 patients with hemiplegia and found normal latencies of both SP1 and SP2 components of this reflex, but reduced amplitude and increased habituation of the SP2 evoked by stimulation of the paretic side. These authors concluded that, though the masticatory nucleus receives bilateral innervation, the contralateral hemisphere should exert [2,4,10,13,14,17] . This is supported by the presence of delayed jaw jerk [6,10,14,16] and the absence of silent periods of the masseter inhibitory reflexes [9,12,13,14,17,26] or 'efferent block' [26] .…”

Section: Discussionmentioning

confidence: 99%

“…These authors concluded that, though the masticatory nucleus receives bilateral innervation, the contralateral hemisphere should exert [2,4,10,13,14,17] . This is supported by the presence of delayed jaw jerk [6,10,14,16] and the absence of silent periods of the masseter inhibitory reflexes [9,12,13,14,17,26] or 'efferent block' [26] . In patients with trigeminal neuropathy, both SP1 and SP2 components of the masseter inhibitory reflexes should be delayed or reduced in size, while a lesion to the masticatory nucleus or motor axons can cause an ipsilateral muscle weakness and a reduction in the voluntary EMG activity, but the reflex inhibition should remain evident [27] .…”

Section: Discussionmentioning

confidence: 99%