2016
DOI: 10.5114/amsad.2016.60799
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A rare neurologic deficiency in HaNDL syndrome: cranial neuropathy

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Cited by 4 publications
(3 citation statements)
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“…Curiously, the transient focal neurological deficits in our patient include agraphia, a feature not previously described in HaNDL patients, expanding the list of clinical deficits already known that includes motor and sensory aphasia, sensory symptoms, weakness, visual symptoms [ 2 ], cranial neuropathy [ 8 ], papilledema and acute elevation of intracranial pressure [ 7 ], disorientation and inattention [ 9 ].…”
Section: Discussionmentioning
confidence: 82%
“…Curiously, the transient focal neurological deficits in our patient include agraphia, a feature not previously described in HaNDL patients, expanding the list of clinical deficits already known that includes motor and sensory aphasia, sensory symptoms, weakness, visual symptoms [ 2 ], cranial neuropathy [ 8 ], papilledema and acute elevation of intracranial pressure [ 7 ], disorientation and inattention [ 9 ].…”
Section: Discussionmentioning
confidence: 82%
“…Although diverse clinical presentations of neurologic deficits are described, involuntary movements have not been reported. Gómez-Aranda presented 50 cases and reported that the most common neurologic deficit was sensory symptom (78% of episodes), followed by aphasia (66%), motor symptom (56%) and visual symptom (12%).2 The uncommon presentations such as confusional state, amnesia and cranial neuropathy have also been described 35. The transient neurologic deficits could occur before or during the headache.2 For our patient, the chorea occurred during the headache, while sensory and weakness occurred before the headache.…”
Section: Discussionmentioning
confidence: 99%
“…The syndrome of transient headache and neurologic deficits with cerebrospinal fluid (CSF) lymphocytosis (HaNDL), also known as pseudomigraine with CSF pleocytosis, is a relatively rare clinical syndrome. HaNDL presents with recurrent transient episodes of headache associated with, or preceded by, neurologic deficits.1 The clinical manifestations of neurologic deficits are variable, but involuntary movements have not been reported 25. Although the etiology and treatment are not entirely clarified, the infectious or postinfectious autoimmune etiology has been favored.6…”
Section: Introductionmentioning
confidence: 99%