Neuromyelitis optica spectrum disorder (NMOSD) is a rare autoimmune astrocytopathy affecting the central nervous system, particularly the optic nerves and spinal cord. Post-infectious triggers, including SARS-CoV-2 (COVID-19), have been increasingly recognized as potential catalysts for this immune-mediated condition. We report the case of a nine-year-old boy who developed AQP4-IgG-positive NMOSD following confirmed SARS-CoV-2 infection. The patient's clinical onset began 1.5 months prior to admission with a seven-day episode of intractable vomiting, indicative of area postrema syndrome (APS). He subsequently presented with a 20-day history of progressive gait weakness, dysarthria, and complex ocular and cranial nerve deficits. Neurological examination revealed a right one-and-a-half syndrome, bilateral sixth cranial nerve paresis, left peripheral facial paresis, profound bulbar dysfunction (including a weak gag reflex and bilateral 12th nerve paresis), lower limb weakness (4/5), gait ataxia, and bilateral extensor plantar responses. Magnetic resonance imaging (MRI) demonstrated extensive central nervous system involvement. Brain MRI revealed typical hyperintense lesions in the periventricular white matter, thalamic-hypothalamic area, midbrain, medulla, and area postrema, alongside bilateral retrobulbar optic nerve enhancement. Spinal imaging confirmed longitudinally extensive transverse myelitis (LETM) spanning the C1-C6 and T2-T6 levels, featuring central gray matter involvement (H-sign) extending into the lateral columns. Cerebrospinal fluid was largely unremarkable. Serological testing confirmed the diagnosis with positive aquaporin-4 (AQP4)-IgG antibodies (cell-based assay (CBA)), positive antinuclear antibodies (ANAs) (1:80), and positive COVID-19 IgG antibodies, while anti-MOG antibodies were negative. Acute targeted immunotherapy was initiated with high-dose intravenous methylprednisolone (30 mg/kg/day for five days). While this achieved complete resolution of his gait abnormalities, visual impairment persisted. He subsequently underwent five sessions of therapeutic plasmapheresis as rescue therapy, resulting in full visual and neurological recovery. The patient was discharged on a maintenance regimen of oral azathioprine (2 mg/kg/day) and biannual intravenous rituximab. A four-month follow-up MRI confirmed dramatic radiologic improvement, with complete resolution of the spinal cord abnormalities. This pediatric case highlights post-COVID-19 NMOSD as a severe but highly treatable neurological emergency. It underscores the critical need for rapid diagnosis through detailed clinical recognition (including preceding APS), advanced radiographic imaging, and targeted serologic evaluation, as well as the efficacy of plasmapheresis for steroid-refractory symptoms to prevent irreversible disability.

Low intensity electrical stimulation of the distal tibial nerve innvervating the plantar foot with pulse trains promotes extensor activity in reduced animal preparations when delivered during the extensor phase. Since enhancing extensor activity could potentially improve weight support after spinal cord injury (SCI), we evaluated if electrical stimulation of the distal tibial nerve or its medial plantar branch enhances/prolongs extensor activity in a locomotor-trained feline model of SCI. With stimulation trains at levels activating large diameter afferents (low-threshold cutaneous/muscle group I afferents) we found no effects on the activity of the extensors and flexors during walking, whereas stimulation levels activating smaller fibers (higher-threshold cutaneous/ muscle group II) were found to increase swing height for stimuli delivered in late stance/early swing. A further increase in stimulus intensity to levels recruiting noxious afferents terminated ongoing stance and produced a flexor withdrawal response of the paw. Muscle reflex responses to low intensity single-pulse stimuli during walking showed a short-latency inhibition in extensor muscles followed by a longer latency excitatory response when stimulation was delivered during stance, and limited responses when delivered during swing. Flexors showed an early-latency excitatory response followed by a weak inhibitory response for stimulation delivered throughout most of the walking cycle. These reflex responses to single pulse stimulation agreed with prior studies. The absence of extensor activity enhancement with low-intensity train stimulation of the distal tibial nerve during stance observed in other preparations may be partially explained by changes in spinal neuronal properties and locomotor networks in chronic spinal cats.

Primitive reflexes are involuntary, brainstem-mediated motor responses present at birth that facilitate neonatal survival and early development. These reflexes emerge during gestation and are fully established in term newborns, supporting critical functions in feeding, protection, and sensorimotor integration. The central nervous system gradually inhibits these reflexes between 4 and 6 months of age as the cortex matures and voluntary motor control develops. However, primitive reflexes may persist beyond expected developmental milestones or reappear in adulthood, signaling neurological dysfunction. The following primitive reflexes can be categorized by function: Oral-feeding reflexes (rooting, sucking): facilitate neonatal nutrition. Protective reflexes (Moro, asymmetric tonic neck reflex): provide defensive responses. Grasp reflexes (palmar, plantar): promote attachment behaviors. Lower extremity reflexes (Babinski, stepping, Galant): support early motor development . In adults, the reemergence of primitive reflexes, termed frontal release signs, indicates frontal lobe pathology or diffuse cerebral dysfunction associated with dementia and neurodegenerative diseases. Understanding the neuroanatomical pathways, developmental timelines, and clinical significance of each primitive reflex enables clinicians to utilize reflex assessment as a sensitive screening tool for neurological integrity across the lifespan.

The myotatic reflex is monosynaptic, induced by the sudden passive muscle belly fiber stretch, and produces a muscle contraction in the agonist muscle or muscle group with simultaneous antagonist muscle (or muscle group) relaxation.[1] As with all reflexes, it is involuntary, reproducible, and likely is positively selected evolutionarily, specifically to prevent the forceful stretching or pulling of a muscle beyond its normal passive range. This reflex also has utility in helping maintain upright posture by detecting postural muscle group stretch and reflexively correcting accordingly in the common cases of leaning or postural instability, which conserves expended energy.[2] Additionally called the deep tendon, stretch, and jerk reflex, the myotatic reflex is a fundamental and essential part of the neurological examination since the work by Joseph Babinski, Wilheim Erb, and William Gowers in the late 1800s.[3][4]

The neurological examination has evolved from rudimentary clinical observations in ancient civilizations to a structured and indispensable tool in modern medical diagnostics. Early contributions from Hippocratic medicine emphasized the brain as the seat of cognition and introduced systematic observation of neurological signs. In the 19[th] century, figures such as Jean-Martin Charcot, Wilhelm Erb, William Gowers, and Joseph Babinski established the foundations of the modern neurological exam through anatomoclinical correlations, standardization of reflex assessment, and structured clinical reasoning. Throughout the 20[th] century, seminal textbooks-such as those by Mills, McKendree, DeJong, and Wartenberg-helped consolidate and disseminate neurological semiology globally. More recently, evidence-based approaches, exemplified by Steven McGee's work, have introduced statistical rigor to bedside examinations. Despite advances in neuroimaging and electrophysiology, examinations remain a cornerstone of clinical neurology, guiding diagnosis, promoting cost-effective care, and reinforcing the doctor-patient relationship.

Introduction The upper lumbar spine is anatomically predisposed to neural compression due to a relatively narrow spinal canal, the presence of the conus medullaris and proximal cauda equina, and reduced segmental mobility. This distinct anatomy can lead to a wide range of clinical presentations, from nonspecific polyradiculopathy to cauda equina syndrome. The variability in symptoms and the unique anatomical features often complicate surgical decision-making. The primary objective of this study was to evaluate the association between upper lumbar disc level (L1-L2, L2-L3, L3-L4) and neurological as well as functional presentation. Secondary objectives included correlation with radiological characteristics and demographic variables. Material and methods A prospective observational study was conducted at Stavya Spine Hospital and Research Institute over a period of one year. Patients meeting the inclusion criteria underwent a comprehensive clinical evaluation, including a history-taking session, physical examination, and assessment using functional scoring systems, such as the Visual Analogue Scale (VAS) and Oswestry Disability Index (ODI). Patients were asked to map their patterns of back and leg pain, and radiological findings were meticulously documented. Results Fifty patients were enrolled consecutively, with an overall mean age of 51.26 ± 14.68 years. Patients with L1-L2 disc herniation were younger (mean age 42.13 ± 11.14 years) compared with those with L3-L4 herniation (54.45 ± 12.24 years). Although patients with L1-L2 disc herniation were younger on average compared with those with L3-L4 herniation, the difference in age across disc levels was not statistically significant. Most L1-L2 disc herniations were classified as Michigan State University (MSU) Type 1B, while L2-L3 and L3-L4 herniations were predominantly MSU Type 2B and Type 3B, respectively. Gait imbalance, extensor plantar response, motor weakness, sensory deficits, reflex changes, and bowel or bladder involvement were more commonly observed in patients with L2-L3 and L3-L4 disc herniations. Conclusion Upper lumbar disc herniation demonstrates level-specific demographic and clinico-radiological patterns. L1-L2 herniations occur in relatively younger patients and are predominantly MSU Type 1B, whereas L2-L3 and L3-L4 herniations are more common in older individuals and are typically larger, classified as MSU Type 2B and 3B. Disc herniations at L2-L3 and L3-L4 levels more frequently present with upper motor neuron-like (epiconus-related) neurological features, including gait imbalance, extensor plantar response, motor weakness, sensory deficits, reflex changes, and bowel or bladder involvement. Recognition of these level-dependent clinical patterns is essential for accurate diagnosis and timely surgical decision-making in upper lumbar disc herniation.

The Gordon reflex was also called the “paradoxical flexor reflex” when Dr. Alfred Gordon first demonstrated the reflex in 1904 at the Philadelphia Neurological Society. The reflex is a clinical sign that can be easily elicited without the use of any equipment. The Gordon reflex describes an extensor plantar response when the calf muscle is squeezed. The Gordon reflex is very simple to complete and can be of use in determining lesion localization. The clinical sign is used to determine whether a lesion of the pyramidal tract exists. The Gordon reflex is closely associated with the Babinski, Chaddock, and Oppenheim reflexes.[1][2] The Gordon reflex can be used when a patient is uncooperative when eliciting the Babinski reflex or patients with very sensitive soles.

Idiopathic spinal cord herniation has traditionally been considered a relatively rare disease. It presents as a slowly progressive myelopathy and necessitates surgical treatment. Herein, we describe a case of idiopathic spinal cord herniation treated with the hammock method. The patient was a 63-year-old male who became aware of numbness in his left toe twelve months prior to his initial visit. At that time, he had difficulty standing on his right leg. Sensation for pain and temperature was decreased in the left half of his body below the navel. Bilateral lower extremity tendon reflexes were hyperactive, and the bilateral Babinski reflex was positive. He also reported a weak urine stream. The Japanese Orthopedic Association (JOA) score for the thoracic spine was 5 out of 11. Magnetic resonance imaging (MRI) revealed a dural defect at the T4 level, with spinal cord extramedullary prolapse and anterior deviation. Computed tomography (CT) myelography revealed a dural defect in the same area. The patient presented with Frankel classification grade C paraplegia and a slowly progressive Brown-Séquard syndrome. He was diagnosed with idiopathic spinal cord herniation. We performed dural patch closure using the hammock method. Transcranial electrically stimulated muscle evoked potentials and somatosensory evoked potentials were used for monitoring during surgery. After a laminectomy from T3 to T6, a mid-longitudinal incision was made through the dura and arachnoid to expose the spinal cord. The denticulate ligaments were dissected bilaterally, and the nerve roots were preserved. Due to severe adhesions, we expanded the cephalic defect. Next, we passed a non-powdered nitrile sheet anteriorly under the spinal cord, suspending it. The adhesions around the defect and the spinal cord were completely removed, and the spinal cord emerged. An expanded polytetrafluoroethylene (ePTFE) sheet was then inserted to replace the nitrile sheet and sutured to the dura mater as a full-perimeter patch to cover the defect. Postoperatively, there was no progression of paralysis, the anterior deviation of the spinal cord disappeared, and no recurrence was observed two years after surgery. Although he still needed a walking stick, his walking speed improved, and his sensory impairment improved. Final JOA score for the thoracic spine was 8 out of 11.

Spinocerebellar ataxia type 28 (SCA28) is characterized by young-adult onset, very slowly progressive gait and limb ataxia resulting in coordination and balance problems, dysarthria, ptosis, nystagmus, and ophthalmoparesis. In most individuals, SCA28 presents as a loss of coordination of lower limbs (unsteadiness, gait ataxia). Less frequently, ptosis/ophthalmoplegia, dysarthria, or upper-limb incoordination may occur as the initial finding. The course of the disease is slowly progressive without impairment of functional autonomy even decades after onset.

A 44-year-old woman had weakness in her right lower limb, a right Babinski reflex, paresthesia in her left lower leg, hypoesthesia at and below the T6 dermatome, and abnormality of the vibrational perception in both legs after prolonged exertion. Her medical history comprised sensorineural hearing loss and diabetes. Furthermore, her child had mitochondrial disease with an m.3243A>G. The patient was diagnosed with maternally inherited diabetes and deafness (MIDD), and the disease-causing variant was identified as m.3243A>G. Cerebrospinal fluid analysis revealed the presence of oligoclonal bands. T2-weighted magnetic resonance imaging showed hyperintensity of the right side of the spinal cord at the level of the 4th thoracic vertebra. This paper examines spinal cord lesions that occur in patients with mitochondrial diseases.

Plantar reflex has been an integral component of neurological examination since its introduction more than a century ago. Despite its simplicity of description, elicitation and interpretation of the reflex and inter-observer agreement have not proven as easily achievable or perfect as the original succinct description promises. We propose a method and a simple tool to grade and standardize performance of plantar reflex among different observers and patients.

Mitochondrial Complex V (ATP synthase) deficiency nuclear type 6 (MC5DN6) is a progressive neurodegenerative disorder characterized by autosomal recessive inheritance and developmental regression, particularly in gross motor skills, which manifests in early childhood. This study aims to present the discovery of a novel variant in four male siblings aged 13 years 9 months to 25 years, making this the fourth family reported globally, while also raising awareness of rare mitochondrial diseases. Four individuals from the same family were retrospectively evaluated based on their demographic, clinical, laboratory, and molecular genetic data. The mutation in the ATP5MK gene was analyzed using the exome sequencing (ES) method. The detected variation was classified according to the criteria American College of Medical Genetics. Four cases, aged between 13 years 9 months and 25 years, were analyzed. All individuals were male. While all four cases had a history of neurodegenerative disease, they also exhibited intellectual disability, muscle weakness, increased deep tendon reflexes in the lower extremities, spasticity, scoliosis, pes cavus deformity, positive Babinski reflex, abnormal gait patterns due to foot deformities, and normal cerebellar tests. Additional findings included geographic tongue (n = 2), strabismus (n = 2), nystagmus (n = 1), ophthalmoplegia (n = 2), hypertrophic upper extremity muscle body build (n = 2), keloid tissue (n = 1), and short stature (n = 3). ES of the first case identified a homozygous splice donor variant (c.87 + 1G > A) in the ATP5MK gene as a novel variant, and family screening revealed the same variant in a biallelic state in the other three siblings. The parents were confirmed as heterozygous carriers, consistent with autosomal recessive inheritance. Mitochondrial diseases can mimic a wide range of neurological disorders. They should be considered as a potential underlying cause when treatment for suspected differential diagnoses proves ineffective.