The sensory ataxia variant of Guillain - Barré syndrome (GBS) is a rare form with an unconfirmed prognosis and clinical course and no documented rehabilitation outcomes. This report describes the clinical course - from onset to discharge - and the rehabilitation details of a patient with sensory ataxic GBS who struggled to regain independent ambulation 6 months after intravenous immunoglobulin (IVIg) therapy. A 75-year-old male was admitted with abnormal sensations and severe limb and trunk ataxia. Owing to the severity of ataxia, the patient was fully dependent on assistance with activities of daily living (ADLs). Muscle strength was mildly weakened in the right hand but was otherwise normal. Cerebrospinal fluid analysis revealed albuminocytologic dissociation, and nerve conduction studies showed poor sensory response conduction. Physical therapy focused on standing and gait training, whereas occupational therapy targeted balance and ADL training. Because sensory recovery was slow, the intervention aimed to maintain muscle strength and joint range of motion, providing maximal assistance during standing and gait activities; the level of assistance was modified according to the patient's response. The patient was transferred to a rehabilitation hospital 33 days after IVIg administration and was discharged 21 weeks later. At that time, the patient could transfer to a wheelchair and move around independently using the wheelchair; additionally, walking was possible with a walker under supervision but independent walking was not possible. The Scale for the Assessment and Rating of Ataxia score improved from 31 to 20. In cases of sensory ataxic GBS with severe ataxia, prevention of functional decline during the acute phase until the observation of reduced ataxia symptoms is critical. The rehabilitation and treatment course described in this case may provide valuable insights for managing patients with sensory ataxic GBS who experience difficulty with recovery. Brainstem stroke represents one of the most devastating forms of cerebrovascular injury, with both ischemic and hemorrhagic subtypes contributing significantly to global morbidity and mortality. Ischemic brainstem stroke occurs more frequently than hemorrhagic variants, yet both are associated with high lethality due to the extraordinary density of nuclei, tracts, and autonomic centers packed within this compact region. Because even small lesions can produce catastrophic neurological deterioration, prompt recognition of brainstem stroke syndromes is essential for improving patient outcomes. Early diagnosis and intervention have been shown to dramatically reduce morbidity and mortality, reinforcing the value of detailed anatomical and clinical knowledge among frontline neurologists, emergency physicians, and neurocritical care teams. The brainstem—comprising the midbrain, pons, and medulla oblongata—is positioned in the posterior cranial fossa and forms the primary conduit between the cerebrum, cerebellum, and spinal cord. Embryologically, it arises from the mesencephalon and portions of the rhombencephalon, originating from the neural ectoderm. Internally, the brainstem is functionally organized into 3 vertical laminae: the tectum, tegmentum, and basis. The tegmentum houses the cranial nerve nuclei, reticular formation, and numerous integrative centers, while the basis contains major ascending and descending white-matter tracts critical for sensorimotor relay. This arrangement allows the brainstem to regulate essential physiological functions—including respiration, cardiac rhythm, blood pressure, consciousness, and the sleep–wake cycle—while also supporting vision, hearing, balance, swallowing, taste, speech, and sensory-motor innervation of the face. The density of gray matter clusters and the compact organization of long tracts mean that even small ischemic lesions can disrupt multiple, simultaneous physiological functions. Because the brainstem’s vascular architecture is region-specific, the clinical manifestations of stroke depend heavily on which territorial distribution is compromised. Each brainstem segment is supplied by a predictable but intricately branching vascular network. For example, the medulla oblongata receives blood from the anterior spinal artery, vertebral artery, posterior inferior cerebellar artery, and posterior spinal artery; the pons receives perforators from the basilar artery as well as branches from the anterior inferior cerebellar and superior cerebellar arteries; and the midbrain is supplied by branches of the posterior cerebral artery, anterior choroidal artery, superior cerebellar artery, and related collicular and choroidal branches. These territories can be conceptualized through the following major groups: Medulla: Anteromedial, anterolateral, lateral, and posterior regions are supplied by the anterior spinal artery, vertebral artery, posterior inferior cerebellar artery (PICA), and posterior spinal artery. Pons: Anteromedial, anterolateral, and lateral pontine zones are supplied by basilar perforators, the anterior inferior cerebellar artery, and the superior cerebellar artery. Midbrain: Anteromedial, anterolateral, lateral, and posterior groups supplied by the posterior cerebral artery, anterior choroidal, superior cerebellar artery, and the collicular or choroidal branches. An understanding of this vascular topology is crucial for identifying lesion patterns, predicting clinical syndromes, and guiding acute management decisions. Brainstem infarctions result from loss of oxygen supply to any of these territories and account for nearly one-third of all ischemic strokes. Pontine infarctions are the most common, whereas medullary infarctions account for approximately 7% of ischemic brainstem strokes, with lateral medullary (Wallenberg) syndrome the predominant subtype.[JAMP. Brainstem Infarcts: Imaging Features and Clinical Presentation] Overall, a notable male preponderance of brainstem stroke has been observed, with a male-to-female ratio of approximately 3:1. Large vessel atherosclerosis, small vessel disease affecting perforating arteries, cardioembolic, and vertebral artery dissection represent the leading etiologies, though basilar artery occlusion remains a critical cause of posterior circulation ischemic strokes.  Pontine strokes may be isolated or may occur as components of broader posterior-circulation infarctions. Ventral pontine infarcts are particularly common and frequently produce classic lacunar syndromes, eg, pure motor hemiparesis, dysarthria-clumsy hand syndrome, ataxic hemiparesis, and pure sensory stroke. In contrast, isolated midbrain infarctions are rare and typically present alongside involvement of adjacent structures, including the cerebellum, pons, or thalamus. Hemorrhagic brainstem stroke most commonly affects the dorsal pons, a region where dense perforator networks make small-vessel rupture particularly devastating.  Among these territories, the pons—the largest brainstem structure, situated between the midbrain and medulla—is especially vulnerable to ischemic injury because of its reliance on numerous small perforating vessels. Disruption of blood flow to the pons can result in pontine infarction, a subtype of ischemic stroke with a broad spectrum of clinical manifestations. Patients may present with classical “crossed” neurological signs, characterized by ipsilateral cranial nerve palsy with contralateral motor or sensory impairment. However, presentations can be highly variable and may include pure motor hemiparesis or hemiplegia, pure sensory stroke, or mixed syndromes such as dysarthria-clumsy hand or ataxic hemiparesis. This heterogeneity directly reflects the tight anatomical juxtaposition of corticospinal tracts, cranial nerve nuclei, transverse pontocerebellar fibers, and reticular activating pathways. Collectively, brainstem strokes remain a uniquely challenging subset of cerebrovascular disease. Their clinical consequences stem from both the complexity of the neuroanatomy and the critical life-sustaining functions localized within this region. A detailed understanding of the structural organization, vascular supply, and clinical correlates is essential for clinicians involved in acute stroke care, neuroimaging interpretation, and neurocritical management. Continued advancements in acute therapy, imaging, and neurovascular intervention underscore the importance of early recognition and precise localization of brainstem infarction patterns to optimize outcomes for this high-risk population.

Anti-GQ1b antibody syndrome (AGABS) unifies triad-defined Miller Fisher syndrome (MFS), Bickerstaff brainstem encephalitis (BBE), and the ophthalmoplegic variant of Guillain-Barré syndrome (GBS-O) under a post-infectious immune mechanism centered on IgG to disialosyl gangliosides. The spectrum also encompasses triad-minus phenotypes-acute ophthalmoparesis without ataxia, acute vestibular syndrome, optic involvement, and acute sensory-ataxic neuropathy. A molecular-mimicry model with complement-mediated nodal/paranodal dysfunction explains severe early deficits despite bland limb nerve conduction studies (NCSs), the cranial/proprioceptive predilection, and generally favorable treatment responsiveness to immunotherapy. In practice, a serology-first strategy, complemented by targeted electrophysiology-blink and H-reflex testing, and, where feasible, paired SEP-ABR showing a literature-supported dissociation (normal ABR with impaired median-nerve cortical SEPs), which, in our series, was documented in one illustrative BBE case-and by structured neuro-otologic examination, mitigates the "normal-NCS trap" and enables timely treatment. Intravenous immunoglobulin (IVIg) is first-line; plasma exchange (PLEX) is an alternative in severe or IVIg-ineligible cases; and intravenous methylprednisolone (IVMP) may be added selectively for central/optic-weighted phenotypes without routine oral taper. We consolidate actionable diagnostic and therapeutic steps and examine them in an institutional series of 16 consecutive seropositive patients (2015-2025): all were anti-GQ1b-positive with frequent GT1a co-reactivity; most reported an antecedent infection-typically upper respiratory, less often gastrointestinal-within the two weeks before onset; limb NCSs were often nondiagnostic whereas reflex/evoked-potential studies were informative; two required intubation in addition to IVIg; outcomes were generally favorable with early immunotherapy. The practical message: order anti-GQ1b at first contact, pair targeted electrophysiology with neuro-otology, and treat early to exploit reversible nodal/paranodal dysfunction.

Mitochondrial encephalomyopathies are multisystem disorders caused by defects in mitochondrial DNA (mtDNA) or nuclear DNA (nDNA). Sensory ataxic neuropathy, dysarthria, and ophthalmoparesis (SANDO) syndrome is a rare manifestation, often associated with POLG mutations. This study identifies a novel POLG mutation in a SANDO patient, validates its pathogenicity, and analyzes the molecular genetics of 61 reported POLG-SANDO cases. After obtaining informed consent, the proband underwent neurological examination, electromyography, muscle/nerve biopsies (histochemical/ultrastructural analyses), and genetic testing (whole-exome sequencing, mtDNA analysis). Pathogenicity of identified POLG variants was assessed in Cas9-mediated primary neuronal models expressing mutant proteins by measuring reactive oxygen species (ROS) levels and mtDNA copy number (qRT-PCR, ND1/APP ratio). Literature searches (PubMed, CNKI, Wanfang, and ClinVar) identified reported POLG mutations and clinical features in SANDO. Clinical and biopsy findings confirmed SANDO syndrome. Genetic analysis revealed compound heterozygous POLG mutations: a novel c.3297G>C (p.W1099C) and a known c.1774C>T (p.L592F). Neurons expressing either mutant exhibited elevated ROS levels (p < 0.05) and reduced mtDNA copy number compared with controls. Literature synthesis identified over 30 SANDO-associated POLG mutations, with p.A467T (31.2%) and p.W748S (22.1%) being the most frequent. The mean age of onset was 31.6 years. We identify a novel pathogenic POLG variant (p.W1099C) causing mitochondrial dysfunction via impaired mtDNA maintenance, expanding the SANDO genetic spectrum. Functional studies confirmed both mutations induce mitochondrial dysfunction (elevated ROS and decreased mtDNA Copy Number), validating their pathogenicity. The compiled mutation profile aids diagnosis of this phenotypically heterogeneous, frequently misdiagnosed disorder.

Though effective, metronidazole poses multiple side effects, especially with prolonged therapy or high dosage. Among these are metronidazole-induced peripheral neuropathy and encephalopathy, which are severely debilitating. We describe a middle-aged man with a liver abscess who was treated with metronidazole 2.4 g/day for nearly 2 months, and who went on to develop dysarthria, ataxic gait and sensory loss, including numbness and burning paraesthesia in his limbs. Neurological assessment comprised nerve conduction studies (NCS) and magnetic resonance imaging (MRI). NCS indicated axonal neuropathy, and MRI revealed T2/FLAIR hyperintensities in the dentate nuclei and corpus callosum, which are indicative of toxic encephalopathy. Symptoms improved considerably after metronidazole was stopped. This case documents the possibility of metronidazole-induced severe neurological sequelae, such as peripheral neuropathy and encephalopathy, especially with high doses (140 gm) or prolonged therapy. Clinicians must remain vigilant for evidence of neurotoxicity in metronidazole-treated patients, especially those on prolonged or high-dose therapy.

Biallelic variants in polyribonucleotide-nucleotidyltransferase-1 (PNPT1) have been associated with a range of phenotypes from syndromic hearing loss to Leigh's syndrome. More recently, heterozygous variants in PNPT1, have been reported in three families with cerebellar ataxia and prominent sensory neuropathy. Whole genome sequencing was performed in two families with autosomal dominant sensory ataxic neuropathy (SAN). Segregating heterozygous splice site (c.2014-3C>G) and nonsense (p.Arg715Ter) variants were detected in both families. All patients initially presented with an isolated SAN clinically and neurophysiologically with subsequent variable cerebellar involvement. We report two heterozygous PNPT1 variants in two families with a predominant SAN, including the novel p.Arg715Ter. This strengthens the argument of PNPT1 causing dominant disease and highlights a new cause for dominantly inherited SAN.