1/9. Ipsilateral facial weakness in upper medullary infarction-supranuclear or infranuclear origin?We describe two patients with upper medullary infarctions showing ipsilateral facial weakness and relative sparing of the upper facial muscles. Electrophysiological follow-up using transcranial magnetic stimulation of the motor cortex in combination with stimulation of the peripheral facial nerve disclosed a supranuclear (corticofacial) tract lesion in one patient and a partial nuclear/infranuclear intra-axial facial nerve lesion in another.- - - - - - - - - - ranking = 1keywords = nerve (Clic here for more details about this article) |
2/9. Ondine's curse in association with diabetes insipidus following transient vertebrobasilar ischemia.Ischemic lesions of the brainstem can lead to complex neurologic deficits. Failure of the automatic control of ventilation (Ondine's curse syndrome) is a possible but rare syndrome following localized brainstem dysfunction. We report on a 49-year-old man with intermittent bradycardia, cranial nerves' dysfunctions and a slight right-sided hemiparesis. An acute brainstem ischemia was diagnosed and treated immediately with high-dose heparin. cerebral angiography revealed a proximal occlusion of the left vertebral artery but a normal right vertebral artery and a hyperplastic right posterior inferior cerebellar artery. Cranial Computed tomography and MRI scan demonstrated multiple ischemic lesions in the posterior circulation. During a 4-week treatment course the patient underwent six episodes of acute severe hypoxia and hypercapnia requiring orotracheal intubation twice and manual ventilation by air mask over a few minutes for four times after a tracheostomy had been performed. Twice a short-term episode of hypothalamic diabetes insipidus was observed following hypoventilation. We conclude that both Ondine's curse syndrome and diabetes insipidus were due to transient vertebrobasilar ischemia.- - - - - - - - - - ranking = 0.5keywords = nerve (Clic here for more details about this article) |
3/9. Benign segmental myoclonus: electrophysiological evidence of transient dysfunction in the brainstem.We present a 66-year-old patient with segmental myoclonus evoked by a brainstem infarction. The myoclonus appeared soon after a cerebrovascular accident and it was evident in the soft palate, jaw, neck, shoulders and upper limbs. brain MRI showed infarction in the left pons and left cerebellum. Small amounts of orally administered clonazepam were remarkably effective. Electroencephalogram (EEG) and auditory brainstem response (ABR) were normal. Somatosensory evoked potential (SSEP) revealed delays in P 14 and N19 recorded at C3 by right median nerve stimulation. These findings were normalized in 4 days. Seg-mental myoclonus is thought to be evoked by olivary hypertrophy following cerebrovascular accident in the brainstem and is said to be resistant to medication. The limited involvement of the brainstem in our patient may account for the transient segmental myoclonus. The prognosis for this type of segmental myoclonus is excellent.- - - - - - - - - - ranking = 0.5keywords = nerve (Clic here for more details about this article) |
4/9. Claude's syndrome in association with posterior cerebral artery stenosis.BACKGROUND: We report a case of a 61 year old man with midbrain infarction causing Claude's syndrome attributable to stenosis of the posterior cerebral artery. CASE DESCRIPTION: The patient presented with a pupil-sparing left third nerve palsy and contralateral ataxia. A background history of treated hypertension and cigarette smoking was obtained. magnetic resonance imaging revealed an area of infarction involving the left medial midbrain. magnetic resonance angiography revealed significant stenosis of the left posterior cerebral artery. Antiplatelet therapy was instituted and the patient made a satisfactory recovery. CONCLUSIONS: This is the first reported case of Claude's syndrome arising in association with stenosis of the posterior cerebral artery. Intracranial large vessel disease should be considered as a potential aetiologic factor in patients with similar midbrain ischaemia.- - - - - - - - - - ranking = 0.5keywords = nerve (Clic here for more details about this article) |
5/9. A patient with reversible pupil-sparing Weber's syndrome.This is a case report of a lady who presented with pupil-sparing Weber's syndrome. She had left oculomotor nerve palsy with normal pupil and right hemiparesis. The patient subsequently made a good recovery. An ischemic lesion of the lower mid-brain was demonstrated on the MRI scan of the brain, which corresponds to the motor nucleus of the oculomotor nerve. The article also describes the neuroanatomy of the oculomotor nerve and how its partial lesions lead to sparing of the pupil. In addition, this case report documents that a pupil-sparing Weber's syndrome could be reversible.- - - - - - - - - - ranking = 1.5keywords = nerve (Clic here for more details about this article) |
6/9. neurocysticercosis presenting as Weber's syndrome.This case report describes a rare, non-epileptic manifestation of neurocysticercosis where a 22-year-old male presented with acute onset right 3rd nerve palsy with left hemiplegia (Weber syndrome). Computerized tomography and magnetic resonance imaging revealed cysticercus granuloma. The patient improved and became asymptomatic with steroid treatment. Recognizing this clinical entity would avoid unnecessary antituberculous treatment and surgical intervention.- - - - - - - - - - ranking = 0.5keywords = nerve (Clic here for more details about this article) |
7/9. trigeminal neuralgia due to pontine infarction.trigeminal neuralgia (TN) is most commonly caused by vascular compression of the trigeminal nerve root entry zone. Secondary trigeminal neuralgia due to ischemic lesion of the pons is very rare. Here we report a patient with a pontine infarct transecting the central trigeminal pathways resulting with trigeminal neuralgia.- - - - - - - - - - ranking = 0.5keywords = nerve (Clic here for more details about this article) |
8/9. Paroxysmal apnea and vasomotor instability following medullary infarction.BACKGROUND: Central hypoventilation and paroxysmal hypertension are uncommon complications of medullary infarction. To our knowledge, the combination of these autonomic complications of medullary stroke has not previously been reported. OBJECTIVE: To describe a patient who experienced life-threatening paroxysmal attacks of central apnea and vasomotor instability 3 months after medullary infarction, a combination of symptoms that is unusual. PATIENT, methods, AND RESULTS: Following a right lateral medullary infarction, an otherwise stable 70-year-old woman developed recurrent episodes of apnea (PCO2), > 100 mm Hg), blood pressure instability (systolic blood pressure, > 200 to < 100 mm Hg), and mental status changes (from agitation to coma) within hours of removal from mechanical ventilation. These attacks occurred repeatedly after removal from mechanical ventilation and were prevented by diaphragm pacing with a phrenic nerve pacemaker and nocturnal mechanical ventilation via a tracheostomy. CONCLUSIONS: A syndrome of life-threatening central hypoventilation and vasomotor instability can occur after medullary infarction. Placement of a phrenic nerve pacemaker can prevent these complications, without the functional limitations imposed by continuous mechanical ventilation.- - - - - - - - - - ranking = 1keywords = nerve (Clic here for more details about this article) |
9/9. Claude's syndrome associated with supranuclear horizontal gaze palsy caused by dorsomedial midbrain infarction.Claude's syndrome caused by dorsal midbrain lesion is characterized by ipsilateral third nerve palsy and contralateral ataxia. To date, reports in the literature concerning Claude's syndrome associated with the midbrain paresis of horizontal gaze are rare. A 62-year-old man suddenly developed left third cranial nerve palsy, right lateral gaze palsy, and right ataxia. Intact Bell's phenomenon and preserved right horizontal oculocephalic reflex suggested the lateral gaze palsy in the right eye was supranuclear in nature. magnetic resonance imaging (MRI) revealed an infarction in the left dorsomedial midbrain. Although the red nucleus has often been suggested as the lesion site responsible for Claude's syndrome, a lesion of the superior cerebellar peduncle just below and medial to the red nucleus could be responsible for this syndrome. This case demonstrates neurological heterogeneity of midbrain infarction.- - - - - - - - - - ranking = 1keywords = nerve (Clic here for more details about this article) |