Motor Palsy Research Articles

Long‐term neurological and functional outcome in Nipah virus infection

Nipah virus (NiV) is an emerging zoonosis. Central nervous system disease frequently results in high case-fatality. Long-term neurological assessments of survivors are limited. We assessed long-term neurologic and functional outcomes of 22 patients surviving NiV illness in Bangladesh. During August 2005 and May 2006, we administered a questionnaire on persistent symptoms and functional difficulties to 22 previously identified NiV infection survivors. We performed neurologic evaluations and brain magnetic resonance imaging (MRI). Twelve (55%) subjects were male; median age was 14.5 years (range 6-50). Seventeen (77%) survived encephalitis, and 5 survived febrile illness. All but 1 subject had disabling fatigue, with a median duration of 5 months (range, 8 days-8 months). Seven encephalitis patients (32% overall), but none with febrile illness had persistent neurologic dysfunction, including static encephalopathy (n = 4), ocular motor palsies (2), cervical dystonia (2), focal weakness (2), and facial paralysis (1). Four cases had delayed-onset neurologic abnormalities months after acute illness. Behavioral abnormalities were reported by caregivers of over 50% of subjects under age 16. MRI abnormalities were present in 15, and included multifocal hyperintensities, cerebral atrophy, and confluent cortical and subcortical signal changes. Although delayed progression to neurologic illness following Nipah fever was not observed, persistent fatigue and functional impairment was frequent. Neurologic sequelae were frequent following Nipah encephalitis. Neurologic dysfunction may persist for years after acute infection, and new neurologic dysfunction may develop after acute illness. Survivors of NiV infection may experience substantial long-term neurologic and functional morbidity.

Post herpetic spinal segmental paralysis

Herpes zoster is a common neurocutaneous viral infection caused by reactivation of varicella zoster virus (VZV) in the sensory ganglia. It is characterized clinically by radicular pain and vesicular cutaneous eruptions in dermatomal distribution [1]. Though, principally a disease of sensory ganglia, motor involvement is not uncommon. However motor involvement generally involves cranial nerves. Motor palsies of spinal roots due to herpes zoster are rarely recorded. Recently we came across a case of post herpetic spinal segmental paralysis which is being reported.

Ulnar Nerve Palsy Associated With Fracture of the Distal Radius

To describe the clinical features and outcome of a series of patients with complete motor and sensory ulnar nerve palsy associated with a fracture of the distal radius. Retrospective case series. Level 1 trauma center. Five adults with acute complete motor and sensory ulnar nerve palsy associated with fracture of the distal radius were treated during a 2 year period. There were 3 men and 2 women, with an average age of 42 years (range, 33 to 56 years). All 5 distal radius fractures were high energy and widely displaced. Three patients had an associated ulna fracture (2 styloid, 1 styloid and distal diaphysis), and 1 had a complete triangular fibrocartilage complex (TFCC) avulsion from the distal ulna (associated with an open wound). Two patients had open fractures. Open reduction and internal fixation of the distal radius fracture in 4 patients and external fixation in 1 patient. Three patients had exploration and release of the ulnar nerve because it was associated with an acute carpal tunnel syndrome. Recovery of ulnar nerve function. At an average follow-up of 17 months, 4 patients had complete or near-complete recovery of ulnar nerve function. One patient had moderate motor and mild sensory dysfunction. Acute ulnar nerve palsy may occur in association with high-energy, widely displaced fractures of the distal radius. These are usually neurapraxic injuries that recover to normal or near-normal strength and sensation. We recommend exploration and release of a complete ulnar nerve palsy associated with a fracture of the distal radius fracture when there is an open wound or an acute carpal tunnel syndrome, and observation without exploration otherwise.

Long-term Results of Expansive Open-Door Laminoplasty for Cervical Myelopathy−Average 14-Year Follow-up Study

Retrospective case series on long-term follow-up results of original expansive open-door laminoplasty for cervical myelopathy due to cervical spondylosis (CSM) and ossification of posterior longitudinal ligament (OPLL). To elucidate efficacy and problems of original open-door laminoplasty to improve future surgical outcomes. Little information is available on long-term outcomes of original open-door laminoplasty without grafts, implants, or instruments. The study group included 80 patients who underwent original open-door laminoplasty and were followed for minimum 10 years. Clinical results, including Japanese Orthopedic Association scores, recovery rates, occurrences of complications, and long-term deterioration were investigated. Cervical alignments, type of OPLL, cervical range of motion, anteroposterior diameter of spinal canal, and progression of OPLL were assessed on plain radiographs. Spinal cord decompression was verified on magnetic resonance imaging. Average Japanese Orthopedic Association score and recovery rate improved significantly until 3 years after surgery and remained at an acceptable level in both cervical spondylosis and OPLL patients with slight deterioration after 5 years. Segmental motor palsy developed in 8 patients. Late deterioration, mainly lower extremity motor score decline, developed in 8 CSM and 16 OPLL patients. Overall cervical range of motion decreased by 36%. Patients with cervical lordosis decreased gradually in both patient groups. Such changes in alignments did not affect surgical results in CSM patients, while OPLL patients with preoperative kyphosis had lower recovery rates than those with straight and lordotic alignments. OPLL progression that was detected in 66% of patients did not affect clinical results. Although infrequent, magnetic resonance imaging revealed atrophy of spinal cord, spinal cord compression at adjacent segments due to degenerative changes and OPLL progression. Long-term results of open-door laminoplasty without bone graft, graft substitutes, or instruments were satisfactory. However, segmental motor paralysis, kyphosis, established before and after surgery, OPLL progression, and late deterioration due to age-related degeneration remain challenging problems.

Validation and Test Characteristics of a 10-Item Neuro-Ophthalmic Supplement to the NEI-VFQ-25

To determine whether a 10-Item Neuro-Ophthalmic Supplement increases the capacity of the 25-Item National Eye Institute Visual Function Questionnaire (NEI-VFQ-25) to capture self-reported visual dysfunction in patients with neuro-ophthalmologic disorders. A cross-sectional survey to examine the characteristics of a 10-Item Neuro-Ophthalmic Supplement to the 25-Item NEI-VFQ-25 in a cohort of patients with neuro-ophthalmologic disorders. The 10-Item Neuro-Ophthalmic Supplement was designed previously by our research group by survey and focus-group methods. In the present study, the NEI-VFQ-25 and 10-Item Supplement were administered concurrently to patients and disease-free control subjects. High-contrast visual acuities with patient usual distance correction were measured with the use of Early Treatment Diabetic Retinopathy Study (ETDRS) charts. Diagnoses for patients (n = 215) included optic neuritis, multiple sclerosis, idiopathic intracranial hypertension, ischemic optic neuropathy, stroke, ocular myasthenia gravis, ocular motor palsies, and thyroid eye disease. Scores for the 10-Item Supplement had a significant capacity to distinguish patients vs disease-free control subjects that was independent of the NEI-VFQ-25 composite score (odds ratio in favor of patient vs control status for 10-point worsening in Supplement scores: 2.7 [95% confidence interval [CI], 1.6, 4.6]; P < .001, logistic regression models that account for NEI-VFQ-25 composite score, age, and gender). Patients with visual dysfunction (binocular Snellen equivalents worse than 20/20) had significantly lower mean scores (9-21 points lower); these differences remained significant after accounting for age and gender (P >or= .001, linear regression). Supplement items and composite scores demonstrated appropriate degrees of internal consistency reliability. The 10-Item Neuro-Ophthalmic Supplement demonstrates a capacity to capture self-reported visual dysfunction beyond that of the NEI-VFQ-25 alone, which supports validity for this new scale. The use of the 10-Item Supplement in clinical trials and epidemiologic studies will examine its capacity to demonstrate treatment effects in longitudinal cohorts.

Transient downbeat nystagmus from West Nile virus encephalomyelitis

Most human West Nile virus (WNV) infections are asymptomatic, but a minority of patients develops neuroinvasive disease, including a poliomyelitis-like syndrome.1 Reported ophthalmologic manifestations include optic neuritis, uveitis, multifocal choroiditis, ocular motor palsies, and opsoclonus.2–4 We cared for a patient with WNV who developed downbeat nystagmus and ocular flutter with acute areflexic quadriparesis. A 64-year-old previously healthy retired steel mill worker presented after 7 days of leg and arm pain and 4 days of progressive weakness. He reported horizontal binocular diplopia, decreased strength, mild dyspnea, and arm tremor. On admission, temperature was 39.2 °C. He was oriented and followed requests. Visual fields were full. Pupils were equal and reactive. He had a mild esotropia in the primary position, with a partial right abduction deficit with right lateral gaze. Downbeat nystagmus was present in primary gaze, and the amplitude increased in up gaze and lateral gaze (video, on the Neurology Web site at www.neurology.org). Pursuit was saccadic in all directions, but particularly in vertical gaze. He had intermittent …

First a third, then a fourth nerve palsy in multiple intracranial aneurysms

Intracranial aneurysms may be a cause of ocular motor dysfunction, the third nerve being more often involved than the two other cranial ocular motor nerves. We report the unusual occurrence of an isolated fourth nerve palsy related to a cavernous carotid aneurysm, angiographically confirmed. The patient already underwent clipping of a ruptured posterior communicating artery aneurysm 17 years earlier, revealed at that time by a third nerve palsy. Endovascular treatment of the cavernous carotid aneurysm was performed, resulting in complete recovery of the palsy. Occurrence of an acquired fourth nerve palsy in a patient with a past history of aneurysm should prompt neurovascular imaging as multiple aneurysms may cause sequential ocular motor palsies.

脳動脈瘤手術ｕｐｄａｔｅ 椎骨脳底動脈系脳動脈瘤手術における術中モニタリング

The efficacy of intraoperative neurophysiological monitoring in vertebro-basilar artery aneurysm (VB-AN) was clinically examined. Since June 2001, intraoperative monitoring was performed in 12 operations for VB-AN. Five operations were for vertebral artery aneurysms: 4 through the lateral suboccipital route and 1 endovascular surgery. Among 5 operations for basilar bifurcation aneurysms, 3 were through the subtemporal route and 2 were by the anterior temporal approach. The other 2 operations were for the posterior cerebral artery aneurysms by the subtemporal approach. Auditory brain stem responses (ABR) were recorded in 5 operations, somatosensory evoked potential in 1 operation, and motor evoked potential (MEP) in 9 operations by 7 of 300～600 (400 in general) V bipolar transcranial (TC) stimulations or 7 of 3～10 mA brain stem direct (BSD) stimulations. In 5 operations, both TCMEP and BSDMEP were used together. Glasgow outcome scales of 12 patients were divided into 6 good recoveries, 2 moderate disabilities, 3 severe disabilities and 1 persistent vegetative state. Among 3 patients with BA aneurysms who had a significant decrease or disappearance of the amplitude of MEP by the temporally occlusions of the BA or both VA, 2 patients have never suffered from the prolonged motor palsy. ABR monitoring seems to be essential in the operation by lateral suboccipital approach since it is very easy and sensitive. It is also applicable in endovascular surgery. TCMEP seems to be useful in VB-AN surgery in which the primary motor cortex connot always be exposed. BSDMEP was successfully recorded in 5 of 7 operations tried and it seems to be a more effective way to monitor motor functioning than TCMEP.

MOTOR NERVE PALSY FOLLOWING PRIMARY TOTAL HIP ARTHROPLASTY

Background: Nerve palsy is a potentially devastating complication following total hip arthroplasty. The purpose of this study was to retrospectively identify risk factors for, and the prognosis associated with, a motor nerve palsy following primary total hip arthroplasty. Methods: Between 1970 and 2000, 27,004 primary total hip arthroplasties were performed at our institution. Forty-seven patients (0.17%) with postoperative motor nerve dysfunction were identified by a review of the complications log of a total joint database. The medical record of each patient provided the data for this study. The average age of the patients was fifty-seven years at the time of surgery. The patients had serial clinical examinations for a minimum of two years, or until neurologic recovery or death. The nerve palsies were classified as complete or incomplete, and only patients with objective motor weakness were included in the study. The limb lengths were measured on preoperative and postoperative radiographs, and those data were then compared with the limb lengths in a matched cohort of patients who had not sustained a nerve injury after a primary total hip arthroplasty. The extent of neurologic recovery, the need for braces or walking aids, and the use of medications for neurogenic pain were evaluated. Results: There were twenty-nine complete motor nerve palsies (sixteen peroneal, eleven sciatic, and two femoral) and eighteen incomplete motor nerve palsies (fourteen peroneal, three sciatic, and one femoral). A preoperative diagnosis of developmental dysplasia of the hip (p = 0.0004) or posttraumatic arthritis (p = 0.01), the use of a posterior approach (p = 0.032), lengthening of the extremity (p < 0.01), and cementless femoral fixation (p = 0.03) were associated with a significantly increased odds ratio for the development of a postoperative motor nerve palsy. Of the twenty-eight patients with a complete palsy who were available for follow-up, only ten (36%) had complete recovery of motor strength, which took an average of 21.1 months. Seven of the eighteen patients with an incomplete palsy fully recovered their preoperative strength. Twenty-one patients required walking aids, and fifteen required permanent use of an ankle-foot orthosis. Five patients required daily medication for chronic neurogenic pain. Conclusions: Motor nerve palsy is uncommon following primary total hip arthroplasty. A preoperative diagnosis of developmental dysplasia of the hip or posttraumatic arthritis, the use of a posterior approach, lengthening of the extremity, and use of an uncemented femoral implant increased the odds ratio of sustaining a motor nerve palsy. The majority of the motor nerve deficits in our series, whether complete or incomplete, did not fully resolve. Level of Evidence: Prognostic Level II. See Instructions to Authors for a complete description of levels of evidence.

Motor Nerve Palsy Following Primary Total Hip Arthroplasty

Nerve palsy is a potentially devastating complication following total hip arthroplasty. The purpose of this study was to retrospectively identify risk factors for, and the prognosis associated with, a motor nerve palsy following primary total hip arthroplasty. Between 1970 and 2000, 27,004 primary total hip arthroplasties were performed at our institution. Forty-seven patients (0.17%) with postoperative motor nerve dysfunction were identified by a review of the complications log of a total joint database. The medical record of each patient provided the data for this study. The average age of the patients was fifty-seven years at the time of surgery. The patients had serial clinical examinations for a minimum of two years, or until neurologic recovery or death. The nerve palsies were classified as complete or incomplete, and only patients with objective motor weakness were included in the study. The limb lengths were measured on preoperative and postoperative radiographs, and those data were then compared with the limb lengths in a matched cohort of patients who had not sustained a nerve injury after a primary total hip arthroplasty. The extent of neurologic recovery, the need for braces or walking aids, and the use of medications for neurogenic pain were evaluated. There were twenty-nine complete motor nerve palsies (sixteen peroneal, eleven sciatic, and two femoral) and eighteen incomplete motor nerve palsies (fourteen peroneal, three sciatic, and one femoral). A preoperative diagnosis of developmental dysplasia of the hip (p = 0.0004) or posttraumatic arthritis (p = 0.01), the use of a posterior approach (p = 0.032), lengthening of the extremity (p < 0.01), and cementless femoral fixation (p = 0.03) were associated with a significantly increased odds ratio for the development of a postoperative motor nerve palsy. Of the twenty-eight patients with a complete palsy who were available for follow-up, only ten (36%) had complete recovery of motor strength, which took an average of 21.1 months. Seven of the eighteen patients with an incomplete palsy fully recovered their preoperative strength. Twenty-one patients required walking aids, and fifteen required permanent use of an ankle-foot orthosis. Five patients required daily medication for chronic neurogenic pain. Motor nerve palsy is uncommon following primary total hip arthroplasty. A preoperative diagnosis of developmental dysplasia of the hip or posttraumatic arthritis, the use of a posterior approach, lengthening of the extremity, and use of an uncemented femoral implant increased the odds ratio of sustaining a motor nerve palsy. The majority of the motor nerve deficits in our series, whether complete or incomplete, did not fully resolve.

Detection of Neuropathy Due to Mycobacterium leprae Using Noninvasive Neurosensory Testing of Susceptible Peripheral Nerves

The prevalence of disability in patients with Hansen disease is related to peripheral nerve dysfunction. This dysfunction, which is due to chronic nerve compression, is the result of invasion of the peripheral nerve by Mycobacteria leprae. This suggests that early identification of M. leprae would be aided by detection of early stages of peripheral nerve compression. Traditional evaluation of peripheral nerve function with monofilaments, electrodiagnostic testing, or by observing motor palsy or digital ulcers unfortunately identifies only late sequelae of peripheral nerve dysfunction. The cutaneous pressure threshold required to identify 1 from 2 static-touch stimuli was obtained with the Pressure-Specified Sensory Device in upper and lower extremities of 51 patients who completed multidrug therapy for Hansen disease. Abnormal peripheral nerve function was identified in each patient and in each of the 120 bilateral nerves that were evaluated. The degree of nerve dysfunction included the range from early to late stages of nerve compression, suggesting that this method of neurosensory testing offers the possibility for early detection of peripheral nerve problems in Hansen disease.

The 57th Annual Meeting of the American Academy of Neurology, Miami, Florida, April 9-16, 2005

The 57th Annual Meeting of the American Academy of Neurology, Miami, Florida, April 9-16, 2005

A case of systemic lupus erythematosus presenting transverse myelitis after an episode of meningitis

A 27-year-old woman suffering from systemic lupus erythematosus was admitted because she had motor and sensory palsy of the lower extremities, neck stiffness, and a fever. Cerebrospinal fluid study indicated meningitis, and magnetic resonance imaging revealed cord swelling and high signals at Th9-Th12 levels. Antibiotics treatment led to resolution of the meningeal signs. Intravenous cyclophosphamide and prednisolone resulted in a partial recovery from the transverse myelitis neurological disturbance.

Compensation of Intraoperative Transcranial Motor-Evoked Potential Monitoring by Compound Muscle Action Potential After Peripheral Nerve Stimulation

It is often difficult to evaluate the results of transcranial motor-evoked potential (TCMEP) monitoring in patients under general anesthesia because these results are strongly affected by anesthetics and muscle relaxants. To exclude effects of muscle relaxants on TCMEP, compound muscle action potential (CMAP) by supramaximum stimulation of the median nerve immediately after transcranial stimulation (300 to 600 V) was recorded in 70 neurosurgical operations. A relative amplitude index (RAI) was defined as the amplitude of TCMEP after the operative procedure divided by the amplitude of TCMEP before the operative procedure. The RAI was calculated and was compensated by the amplitude of CMAP in 141 limbs. In 12 limbs of 7 patients with postoperatively progressed motor paresis, the compensated RAI was less than 0.2. The compensated RAI in all other 129 limbs of 63 patients without postoperative motor palsy was more than 0.2. These results suggest that compensation of TCMEP monitoring by CMAP is an easy and accurate method for removing the effects of muscle relaxants in TCMEP.

Paralysies oculomotrices douloureuses : une approche diagnostique

We review the question of diagnosis of painful and relatively isolated ophthalmoplegia due to diseases affecting the ocular motor nerves. For each clinical setting, we provide an overview of the main causes and a practical way to approach the diagnosis. As vascular malformations should always be kept in mind in patients with painful ophthalmoplegia, emergency neuroradiological investigations may be needed. However, the etiological scope is wide and the rationale for choosing the more appropriate examination and its optimal timing depends exclusively on the clinical evaluation. Despite advances in investigation techniques, diagnosis may remain difficult or even unresolved in a certain number of patients. We discuss successively paralysis of the third, sixth and fourth nerve, paralysis of several ocular motor nerves, recurrent ophthalmoplegia and ischaemic ocular motor palsies, which are the most frequent cause.

Prophylaxis of C5 palsy after cervical expansive laminoplasty by bilateral partial foraminotomy

Background context It is known that postoperative motor palsy at the C5 level occurs with anterior decompression or posterior decompression and has a relatively good prognosis, but the pathogenesis and possible prophylactic measures of the palsy remain unknown. Purpose The purpose of this study was to evaluate the effectiveness of bilateral partial foraminotomy for preventing C5 palsy from occurring after cervical decompression surgery. Study design A retrospective review was performed concerning the risk factors of the C5 palsy based on the preoperative clinical findings. To investigate the prophylactic effect of the partial foraminotomy, we examined a difference of an incidence of the C5 palsy by performing concurrent partial foraminotomy with expansive laminoplasty. Patient sample A total of 305 cases of cervical expansive laminoplasty performed for spondylotic myelopathy or ossification of the posterior longitudinal ligament were reviewed. Methods We analyzed 305 cases of cervical expansive laminoplasty to investigate the preoperative risk factors that may cause postoperative C5 palsy. To clarify the relationship of the foraminotomy and development of the C5 palsy, we examined 230 patients in whom foraminotomy could be confirmed by operative records. Results Of the 305 patients, postoperative C5 palsy occurred in 13 patients (4.3%): 10 patients had radicular pain (77%), and 8 patients had sensory disturbances (62%). We assessed all neurological findings and X-ray, computed tomography and electromyographic findings, but no statistical differences were found in any of the preoperative clinical findings relative to the occurrence of postoperative C5 palsy. For the open side, 108 cases underwent foraminotomy and 122 cases did not, whereas on the hinge side, 54 cases received foraminotomy and 176 cases did not. In order to investigate the prophylactic effect of foraminotomy, we totaled the open side and hinge side, and calculated the number of bone gutters: 162 gutters had concurrent foraminotomy and 298 gutters did not. Postoperatively, C5 palsy occurred in 1 gutter (0.6%) in the former group and in 12 gutters (4.0%) in the latter group (p<.05, Fisher's direct method). Conclusions There were no specific risk factors among the preoperative clinical findings related to C5 palsy. Bilateral partial foraminotomy was effective for preventing C5 palsy.

Transsphenoidal diplopia

A 46-year-old man developed a pupil-involving incomplete third cranial nerve palsy after undergoing transsphenoidal resection of a pituitary macroadenoma. A CT scan 1 week later revealed postoperative changes, with no new mass lesion, hemorrhage, or orbital fracture. The third cranial nerve palsy spontaneously improved over the ensuing week. Postoperative ocular motor palsy is an uncommon complication of transsphenoidal pituitary surgery. Neuro-imaging should be performed to exclude the presence of a new compressive lesion.

Radial nerve palsy associated with high-energy humeral shaft fractures

Purpose To determine whether the radial nerve should be explored when there is a complete sensory and motor deficit after a high-energy fracture of the humeral diaphysis. Methods Twenty-four patients aged 16 years or older with a high-energy, diaphyseal fracture of the humerus and complete motor and sensory radial nerve palsy were reviewed retrospectively. Eleven fractures were open—6 of these were part of a very complex upper-extremity injury (multiple ipsilateral fractures in 3 patients and near amputation in 3). All 11 patients with open fractures and 3 of 13 patients with closed injuries had radial nerve exploration. Results All 6 patients with a transected radial nerve had an open humerus fracture and were part of a complex upper-extremity injury. Five of 6 had primary repair of the radial nerve, and none recovered. All 8 intact explored nerves and 9 of 10 unexplored nerves recovered; the only nonrecovery occurred in a patient treated with closed intramedullary rod fixation who may have had iatrogenic nerve injury. The average time to initial signs of recovery was 7 weeks (range, 1–25 weeks). The average time to full recovery was 6 months (range, 1–21 months). Conclusions Transection of the radial nerve is usually associated with open fractures of the humerus that are part of a very complex upper-extremity injury. The results of primary nerve repair in this circumstance are poor, likely related to an extensive zone of injury and the need for nerve grafting. Intact nerves and nerve palsies that are part of a closed fracture nearly always recover, even after high-energy injuries. Because the first signs of nerve recovery and complete recovery of the nerve can be quite delayed, patience is merited before considering tendon transfers.

Adaptations and deficits in the vestibulo-ocular reflex after peripheral ocular motor palsies.

Palsy of a nerve might be expected to lower vestibulo-ocular reflex (VOR) responses in its fields of motion, but effects of peripheral neuromuscular disease were unknown. We recorded the VOR during sinusoidal head rotations in yaw, pitch, and roll at 0.5-2 Hz and static torsional gain in 43 patients with unilateral nerve palsies. Sixth nerve palsy (n = 21) reduced both abduction and adduction VOR gains in darkness. In light, horizontal visually enhanced VOR (VVOR) gains were normal in moderate and mild palsy. In severe palsy, horizontal VVOR gains remained low in the paretic eye when it was fixating, whereas gains in the nonparetic eye became higher than normal. Third nerve palsy (n = 10) decreased VOR and VVOR gains during abduction, adduction, elevation, depression, extorsion, and intorsion. Fourth nerve palsy (n = 13) reduced VOR gains of the paretic eye during intorsion, extorsion, elevation, depression, abduction, and adduction, but in light vertical and horizontal VVOR gains were normal. In the nonparetic eye, all gains were normal. Reduced VOR gains in the direction of paretic muscles and also in the direction of their antagonists, together with normal gains in the nonparetic eye, indicate a selective adjustment to the antagonists of paretic muscles. Increase of VVOR gains to normal in the paretic eye, when used for fixation, without conjugate increase in gains in the occluded nonparetic eye, provides further evidence of selective adaptation for the paretic eye. Motions of the eyes after nerve palsies indicate monocular VOR adaptation in three dimensions.

Seventh nerve palsies may be the only clinical sign of small pontine infarctions in diabetic and hypertensive patients.

Small brainstem infarctions are increasingly recognized as a cause of isolated ocular motor and vestibular nerve palsies in diabetic and/or hypertensive patients. This raises the question whether there are also isolated 7(th) nerve palsies due to pontine infarctions in patients with such risk factors for the development of cerebrovascular diseases. Over an 11-year-period, we retrospectively identified 10 diabetic and/or hypertensive patients with isolated 7(th) nerve palsies and electrophysiological abnormalities indicating pontine dysfunction. All patients had examinations of masseter and blink reflexes, brainstem auditory evoked potentials, direct current electro-oculography including bithermal caloric testing, and T1- and T2-weighted MRI (slice thickness: 4-7 mm). Electrophysiological abnormalities on the side of the 7(th) nerve palsy included delayed masseter reflex latencies (4 patients), slowed abduction saccades (4 patients), vestibular paresis (2 patients), and abnormal following eye movements (2 patients). Electrophysiological abnormalities were always improved or normalized at re-examination, which was always associated with clinical improvement. MRI revealed an ipsilateral pontine infarction in 2 patients. Another 2 had bilateral hyperintense intrapontine lesions, and one an ipsilateral cerebellar infarction. Simultaneous improvement or recovery of abnormal clinical and electrophysiological findings strongly indicated that both were caused by the same actual pontine lesions. A 7(th) nerve palsy may be the only clinical sign of a pontine infarction in diabetic and/or hypertensive patients. Such mechanism may be underestimated if based on MRI only.