Physiotherapy in Postinfection Injury to Cranial Nerves III, IV, and VI: A Case Study.

The patient with bacterial infection sequelae in the form of damage to cranial nerves III, IV, and VI was followed up. He had exhibited clinical and radiographic signs of paranasal sinusitis. Before his physiotherapy, the patient received standard treatment with natural and synthetic antibiotics and steroids. After acute signs of infection resolved without any functional improvement, the patient was referred to a rehabilitation unit to undergo neuromuscular re-education of the paralyzed extraocular muscles. Periorbital hydrocortisone iontophoresis and visuomotor exercises with intense ideomotor stimulation led to complete and rapid resolution of extraocular muscle paralysis and diplopia. Physiotherapy can be an effective treatment of choice after failed pharmacological treatment in patients with damage to cranial nerves III and VI. It has many theoretical advantages, including noninvasiveness and avoidance of first-pass metabolism of drugs administered systemically.

Comparing Hypertropia in Upgaze and Downgaze Distinguishes Congenital From Acquired Fourth Nerve Palsies.

BACKGROUND: Isolated fourth nerve palsies are commonly caused by decompensation of a congenitally dysfunctional superior oblique muscle ("decompensated congenital palsies"). Distinguishing such palsies at initial presentation from palsies caused by presumed microvascular ischemia ("ischemic palsies") has value for patient reassurance and in forestalling ancillary testing. Abnormally large vertical fusional amplitudes traditionally have been used to identify decompensated congenital palsies, but that may not be a reliable distinguishing feature. This study was undertaken to determine if the amount of hypertropia in upgaze and downgaze might be a more efficient separator. We also studied traumatic and tumorous fourth nerve palsies to see if they could be distinguished from decompensated congenital palsies by using this hypertropia comparison. METHODS: Retrospective review of case records of patients diagnosed with isolated fourth nerve palsies at the University of Michigan Neuro-Ophthalmology Clinics over the past 15 years. We recorded the age, gender, vascular risk factors, duration of follow-up, cause, side of palsy, and alignment measurements in all patients. RESULTS: Inclusion criteria were met by 118 patients. Hypertropia was equal or greater in upgaze than downgaze in 50 of the 58 decompensated congenital palsies (86%) in whom those data were recorded. Hypertropia was never greatest in upgaze in the 15 patients with traumatic palsies. Vertical fusional amplitudes were increased in only 15 of 27 patients (56%) with decompensated palsies in whom those data were recorded. Torsional misalignment on double Maddox rod testing was present in 16 (94%), 13 (87%), and 3 (100%) patients with ischemic, traumatic, and tumorous palsies, but also in 19 patients (54%) with decompensated congenital palsies in whom those data were recorded. CONCLUSIONS: Hypertropia greater in upgaze than downgaze or equal in upgaze and downgaze was an efficient separator of congenital from ischemic and tumorous fourth nerve palsies, being characteristic of patients with decompensated congenital palsies and never present in patients with ischemic, traumatic, or tumorous palsies. Vertical fusional amplitudes and torsional misalignment did not effectively differentiate between the patient groups. Comparing the hypertropia in upgaze and downgaze improved differential diagnosis and reduces the potential for unnecessary ancillary tests.

Persistent diplopia and superior oblique muscle dysfunction following dissection of the orbital periosteum in cranial base surgery.

BACKGROUND/AIMS: Persistent diplopia secondary to a fourth cranial nerve palsy is poorly documented after open cranial base surgery. METHODS: Six cases of fourth cranial nerve palsy after cranial base surgery were drawn from the Neuro-Ophthalmology and Head and Neck Surgery Clinics at the University of Michigan from 2004 to 2012. RESULTS: Six patients developed diplopia and ocular misalignment in a pattern suggestive of superior oblique palsy following dissection of the medial orbital periosteum as part of a surgical approach to the anterior cranial base. Among the four patients in whom follow-up examination was available, the misalignment improved spontaneously in three patients and was stable in the fourth patient, but did not completely resolve in any patient. CONCLUSIONS: This sparsely documented phenomenon is likely caused by dysfunction of the superior oblique muscle, possibly the result of malposition of the trochlea after spontaneous reattachment of the periosteum. Special factors such as invasive tumours, repeated surgeries of this nature, prior radiation, or chemical cementing material that adversely affects wound healing may be contributory.