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Neuro-ophthalmology
Published in Mostafa Khalil, Omar Kouli, The Duke Elder Exam of Ophthalmology, 2019
A bilateral idiopathic condition characterized by involuntary contraction of the orbicularis oculi muscle due to basal ganglia dysfunction. Presentation is in the sixth decade of life, with a female predominance. Blepharospasm and oromandibular dystonia can occur together in Meige syndrome.
Malformations of the Lymphatic System
Published in Waldemar L. Olszewski, Lymph Stasis: Pathophysiology, Diagnosis and Treatment, 2019
The hereditary lymphedemas thus usually develop spontaneously, without a preliminary inflammatory stage. In the clinical foreground as a congenital form are Nonne-Milroy syndrome and, as a retarded form appearing around the time of puberty, Meige syndrome. The term Meige’s trophedema was selected by the person describing it for the first time, because he thought pathogenetically of a central nervous regulation center. At the present time, it is certain that the peripheral trophicity is ultimately also disturbed; this has been shown, for example, for chronic venous insufficiency by May,10 with venous decompensation being followed by lymphatic decompensation and, finally, also by degeneration of the nerves and ganglia. The lymphedema should be differentiated from phlebolymphatic edema, and especially from elephantiasis-like changes developing after long-lasting venous insufficiency. The Stemmer’s sign is useful in discriminating lymphedema from elephantiasis. In the upper limbs “yellow nails” syndrome is helpful in differential diagnosis. In a noteworthy observation of our own (see Figure 3), rudimentary viscerocutaneous lymphangiectases on the skin of the scrotum and legs had led to monstrous elephantiasis, but the same ectasias intestinally localized (and so demonstrated) had led to an “exudative enteropathy”, that is, to enteral protein losses through an insufficiency of the lymphatic discharge (protein-losing syndrome).
Diagnosis and Differential Diagnosis
Published in Marc H. De Baets, Hans J.G.H. Oosterhuis, Myasthenia Gravis, 2019
In various myopathies, ptosis is slowly developing over years, bilateral, nearly symmetrical and rarely the chief complaint of the patient, except in the chronic progressive external ophthalmoplegia (CPEO). Confusing is the pseudoptosis in extrapyramidal disorders, especially at the onset of the Meige syndrome.135 These patients are not aware of active closure or spasm of the eyelids but report very fluctuating drooping of the eyelids. This may be influenced by “tricks,” such as laying down, vigorous chewing, manual work, or changing of environment. Their complaints are often worse in the course of the day and may react promptly but short-lasting to a new drug, e.g., pyridostigmine per os or Tensilon, as was my own experience. Not exceptionally some blepharospasm is also seen in MG patients with ptosis and the coexistence of MG and Meige has been reported.135
Psychogenic blepharospasm associated with Meige’s syndrome: a case report
Published in Psychiatry and Clinical Psychopharmacology, 2018
Cagdas Oyku Memis, Mustafa Kurt, Gulgez Kerimova, Bilge Dogan, Doga Sevincok, Levent Sevincok
Meige’s syndrome is an adult-onset idiopathic dystonic movement disorder that involves symmetrical blepharospasm, dystonia of lower facial, jaw, tongue, and neck muscles. Symptoms usually begin in the fifth or sixth decade of life with a two-fold predominance of women. Blepharospasm is the most frequent initial complaint of patients, while the other dystonic movements may gradually develop [1]. In majority of cases, Meige’s syndrome develops secondary to structural lesions of the basal ganglia or the rostral brainstem [2]. Meige’s syndrome has been reported to be induced by several antipsychotics, including risperidone, olanzapine, quetiapine, and aripiprazole [1,3]. It was previously reported that Botulinum toxin (BTX) injections had only a moderate improvement rates for Meige’s syndrome [1]. The other treatment options in Meige’s syndrome include anticholinergics, benzodiazepines, baclofen, and tetrabenazine [4].
Experience to prevent wire tethering in deep brain stimulation from a single center
Published in Neurological Research, 2021
Dongliang Wang, Jiayu Liu, Qingpei Hao, Hu Ding, Bo Liu, Zhi Liu, Haidong Song, Jia Ouyang, Ruen Liu
Diagnostic criteria were as follows: (1) Meige syndrome: (a) idiopathic cranial cervical dystonia (blepharospasm and lower facial and oromandibular dystonia, with or without the involvement of cervical muscles); (b) severe functional impairment despite medical management, including failed botulinum toxin therapy; (c) with a disease duration ≥3 years; (d) no history of exposure to neuroleptics; (2) primary PD: (a) with a disease duration ≥5 years; (b) treatment with the best available drugs to good effect previously, but with obviously decreased efficacy at admission, or the presence of movement disorders that affect the quality of daily life; (c) Hoehn–Yahr 2.5–4 stage during the PD-off period, with a total daily off duration ≥4 hours.
Atypical Blepharospasm with Oromandibular Dystonia Associated with Cerebral Amyloid Angiopathy
Published in Neuro-Ophthalmology, 2022
Andrew R. Carey, Neil R. Miller
Benign essential blepharospasm and its related disorder, blepharospasm with oromandibular dystonia (also known as Meige’s syndrome) are dystonic disorders of the facial nerves marked by tonic-clonic spasms of the facial muscles.1 The pathophysiology of the conditions is thought to be related in large part to dysfunction of the thalamus and the basal ganglia, including the globus pallidus, striatum, and the substantia nigra.1 The thalamus normally stimulates the motor cortex to produce normal movements, whereas the globus pallidus normally inhibits the thalamus to prevent unwanted movements, and the striatum normally inhibits the globus pallidus so that the globus pallidus will not cause excessive inhibition of the thalamus. Finally, the substantia nigra normally stimulates the striatum by releasing dopamine. If the substantia nigra stops exciting the striatum, the striatum stops inhibiting the globus pallidus, and the globus pallidus stops inhibiting the thalamus. Loss of inhibition of the thalamus results in unwanted movements in various parts of the body, including the face, neck, and throat.2 Despite laboratory evidence for this mechanism in patients with essential blepharospasm and Meige’s syndrome, neuroimaging studies of these regions in patients with these conditions typically show no structural lesions.3 We report the first case of blepharospasm associated with cerebral amyloid angiopathy (CAA). The imaging findings in this case support the above mechanism and emphasises the importance of obtaining appropriate magnetic resonance imaging (MRI) sequences in patients with blepharospasm, particularly when there are atypical features.