Recovery From Homonymous Hemianopia in Hyperglycemia-Induced Occipital Lobe Electroclinical Seizures Following Glycemic Control.

BACKGROUND: Visual changes due to hyperglycemia in diabetes are not uncommon. While blurred vision is a well-established sequela of chronic hyperglycemia, homonymous hemianopia with or without electroclinical seizures is much rarer and can be mistaken for migraine, temporal arteritis, or ischemia of the central nervous system. METHODS: This article analyzed case studies for 3 patients (67M, 68M, 52F) presenting with complex visual phenomena, from 3 to 42 days duration, including pathogenesis, clinical findings, management, and follow-up. RESULTS: Examinations demonstrated dense left homonymous hemianopias in 2 patients and a left inferior homonymous quadrantanopia in one, with no other abnormalities. Patients described vivid, nonstereotyped intermittent hallucinations in the affected fields. Blood glucose levels ranged from 13.5 to 35.0 mmol/L (243-630 mg/dL) without ketosis and HbA1c from 14.6% to 16.8%. Computed tomography of the brain showed no acute intracranial pathology. MRI of the brain either detected no abnormalities or demonstrated changes consistent with seizure activity. Electroencephalogram (EEG) demonstrated seizures over the right occipital region in each patient. EEG seizures coincided with patients' hallucinations, while they remained otherwise conscious. Oral hypoglycemic and antiepileptic medications were commenced with rapid and complete reversal of the seizures and visual field deficits, confirmed by repeat Automated 30-2 and MRI. CONCLUSIONS: Hyperglycemia-induced occipital lobe seizures with visual hallucinations and interictal homonymous visual field defects represent a rare but clinically important diagnosis. This article highlights the importance of prompt recognition and treatment to facilitate recovery.

Nitrous oxide-induced myeloneuropathy.

BACKGROUND AND PURPOSE: Nitrous oxide misuse is a recognized issue worldwide. Prolonged misuse inactivates vitamin B12, causing a myeloneuropathy. METHODS: Twenty patients presenting between 2016 and 2020 to tertiary hospitals in Sydney with myeloneuropathy due to nitrous oxide misuse were reviewed. RESULTS: The average age was 24 years, and mean canister consumption was 148 per day for 9 months. At presentation, paresthesias and gait unsteadiness were common, and seven patients were bedbound. Mean serum B12 was normal (258 pmol/L, normal range [NR] = 140-750) as was active B12 (87 pmol/L, normal > 35). In contrast, mean serum homocysteine was high (51 µmol/L, NR = 5-15). Spinal magnetic resonance imaging (MRI) showed characteristic dorsal column T2 hyperintensities in all 20 patients. Nerve conduction studies showed a predominantly axonal sensorimotor neuropathy (n = 5). Patients were treated with intramuscular vitamin B12, with variable functional recovery. Three of the seven patients who were bedbound at presentation were able to walk again with an aid at discharge. Of eight patients with follow-up data, most had persistent paresthesias and/or sensory ataxia. Mobility scores at admission and discharge were not significantly correlated with the serum total and active B12 levels or cumulative nitrous oxide use. There were no significant trends between serum active B12 level and cumulative nitrous oxide use (Spearman rho = -0.331, p = 0.195). CONCLUSIONS: Nitrous oxide misuse can cause a severe but potentially reversible subacute myeloneuropathy. Serum and active B12 can be normal, while elevated homocysteine and dorsal column high T2 signal on MRI strongly suggest the diagnosis. Neurological deficits can improve with abstinence and B12 supplementation, even in the most severely affected patients.

Dual processing of visual rotation for bipedal stance control.

KEY POINTS: When standing, the gain of the body-movement response to a sinusoidally moving visual scene has been shown to get smaller with faster stimuli, possibly through changes in the apportioning of visual flow to self-motion or environment motion. We investigated whether visual-flow speed similarly influences the postural response to a discrete, unidirectional rotation of the visual scene in the frontal plane. Contrary to expectation, the evoked postural response consisted of two sequential components with opposite relationships to visual motion speed. With faster visual rotation the early component became smaller, not through a change in gain but by changes in its temporal structure, while the later component grew larger. We propose that the early component arises from the balance control system minimising apparent self-motion, while the later component stems from the postural system realigning the body with gravity. ABSTRACT: The source of visual motion is inherently ambiguous such that movement of objects in the environment can evoke self-motion illusions and postural adjustments. Theoretically, the brain can mitigate this problem by combining visual signals with other types of information. A Bayesian model that achieves this was previously proposed and predicts a decreasing gain of postural response with increasing visual motion speed. Here we test this prediction for discrete, unidirectional, full-field visual rotations in the frontal plane of standing subjects. The speed (0.75-48 deg s(-1) ) and direction of visual rotation was pseudo-randomly varied and mediolateral responses were measured from displacements of the trunk and horizontal ground reaction forces. The behaviour evoked by this visual rotation was more complex than has hitherto been reported, consisting broadly of two consecutive components with respective latencies of ∼190 ms and >0.7 s. Both components were sensitive to visual rotation speed, but with diametrically opposite relationships. Thus, the early component decreased with faster visual rotation, while the later component increased. Furthermore, the decrease in size of the early component was not achieved by a simple attenuation of gain, but by a change in its temporal structure. We conclude that the two components represent expressions of different motor functions, both pertinent to the control of bipedal stance. We propose that the early response stems from the balance control system attempting to minimise unintended body motion, while the later response arises from the postural control system attempting to align the body with gravity.