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Case Report: Unilateral Hemispheric Hemorrhage with Bilateral Ptosis and Upgaze Palsy

Wong KH, Yong MH, Mohd Khialdin S, Wan Abdul Halim WH

Optom Vis Sci, 2023 Dec 01;100(12):895-899.

PMID: 38019959 DOI: 10.1097/OPX.0000000000002089

SIGNIFICANCE: Determining the anatomic location of insult in cases of concurrent bilateral upgaze palsy with bilateral ptosis can be challenging because of the various overlapping pathways and shared functions. It is more commonly related to bilateral oculomotor nerve palsies and myasthenia gravis. However, the possibility of unilateral cerebrovascular events may be overlooked because of the lack of laterality of disease manifestations.

PURPOSE: This report documents the uncommon presentation of bilateral ptosis and upgaze palsy in unilateral hemispheric hemorrhage with the corresponding clinical and anatomical review.

CASE REPORT: A 46-year-old gentleman presented to the emergency department with left-sided hemiplegia, concurrent bilateral ptosis, and upgaze palsy. He was found to have acute hemorrhagic stroke secondary to significantly elevated blood pressure. Computed tomography of the brain revealed acute extensive intraparenchymal hemorrhage involving the right basal ganglia, frontal lobe, and temporal lobe. There was an extension of hemorrhage into the third ventricle and subarachnoid extension to the Sylvian fissure with obstructive hydrocephalus. An emergency right craniotomy was performed to evacuate the blood clot, and the hydrocephalus subsequently resolved. Post-operatively, bilateral ptosis and upgaze palsy improved and then resolved.

CONCLUSIONS: Acute bilateral ptosis and upgaze palsy suggest the possibility of unilateral hemispheric hemorrhage, even though there is no direct involvement of the brainstem and its nuclei.

Matched MeSH terms: Paralysis/complications

Acute flaccid paralysis with chronic cough

Chai CH, Yuki N, Nor HM, Goh KJ, Shahrizaila N

Pract Neurol, 2012 Oct;12(5):328-31.

PMID: 22976064 DOI: 10.1136/practneurol-2011-000205

Matched MeSH terms: Paralysis/complications*

Congenital bilateral facial nerve hypoplasia with sensorineural hearing loss: a case report

Hamizan AW, Yean KT, Abdullah A

Int J Pediatr Otorhinolaryngol, 2012 Mar;76(3):455-9.

PMID: 22281372 DOI: 10.1016/j.ijporl.2012.01.002

A 3-year-old child presented with congenital bilateral facial nerve palsy with bilateral profound sensorineural hearing loss. High Resolution Computed Tomogram (HRCT) of the temporal bones found bilateral atresia of cochlear nerve canals, incomplete partition of the cochleae and narrow facial nerve canals. Magnetic resonance imaging (MRI) revealed bilateral hypoplasia of facial nerves and aplasia of both vestibulocochlear nerves. There have been no other reported cases with this presentation. The possible aetiology and treatment options for the patient are discussed. We highlighted the review of aplasia/hypoplasia of the facial nerve and hypoplasia of cochlear nerve canal.

Matched MeSH terms: Facial Paralysis/complications*

Fulltext Recurrent Bell's palsy in a young woman

Ngow HA, Wan Khairina WM, Hamidon BB

Singapore Med J, 2008 Oct;49(10):e278-80.

PMID: 18946598

Bell's palsy is a benign lower motor neuron facial nerve disorder. It is almost always unilateral. We report a 20-year-old nulliparous woman with five episodes of recurrent Bell's palsy. A review of recent medical literature revealed a paucity of case reports involving an individual with five episodes of recurrent Bell's palsy, with none found in Asian neurology medical literature. Despite the multiple episodes of Bell's palsy recurrences, the patient did not suffer much neurological sequelae from the disease.

Matched MeSH terms: Facial Paralysis/complications

Thyrotoxicosis presenting as hypokalaemic paralysis and hyperlactataemia in an oriental man

Al-Jubouri MA, Inkster GD, Nee PA, Andrews FJ

Ann. Clin. Biochem., 2006 Jul;43(Pt 4):323-5.

PMID: 16824287 DOI: 10.1258/000456306777695681

A 35-year-old Malaysian man presented with rapid onset of flaccid quadriparesis associated with nausea and vomiting. General blood tests revealed severe hypokalaemia (serum potassium 1.5 mmol/L) and hypophosphataemia (serum phosphate 0.29 mmol/L) as a potential cause of the flaccid paralysis. Arterial blood gases showed mixed acid base disturbance of respiratory alkalosis and metabolic acidosis with hyperlactataemia. Thyrotoxic periodic paralysis (TPP) was suspected as the underlying cause of this presentation and thyroid function tests showed severe hyperthyroid results (free T4 > 77.2 pmol/L, free T3 19.3 pmol/L, thyroid-stimulating hormone [TSH] < 0.05 mIU/L). Treatment with intravenous potassium and phosphate infusion and oral propranolol resulted in rapid resolution of his symptoms. A discussion of the clinical and pathophysiological features and treatment of TPP (a very rare encounter in UK clinical practice) is presented, and to our knowledge associated hyperlactataemia has not been previously described.

Matched MeSH terms: Hypokalemic Periodic Paralysis/complications

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