The cerebellum acts as the analog to the medial temporal lobe for sensorimotor memory.

The cerebellum is critical for sensorimotor learning. The specific contribution that it makes, however, remains unclear. Inspired by the classic finding that for declarative memories, medial temporal lobe (MTL) structures provide a gateway to the formation of long-term memory but are not required for short-term memory, we hypothesized that for sensorimotor memories, the cerebellum may play an analogous role. Here, we studied the sensorimotor learning of individuals with severe ataxia from cerebellar degeneration. We dissected the memories they formed during sensorimotor learning into a short-term temporally-volatile component, that decays rapidly with a time constant of just 15 to 20 s and thus cannot lead to long-term retention, and a longer-term temporally-persistent component that is stable for 60 s or more and leads to long-term retention. Remarkably, we find that these individuals display dramatically reduced levels of temporally-persistent sensorimotor memory, despite spared and even elevated levels of temporally-volatile sensorimotor memory. In particular, we find both impairment that systematically worsens with memory window duration over shorter memory windows (<12 s) and near-complete impairment of memory maintenance over longer memory windows (>25 s). This dissociation uncovers a unique role for the cerebellum as a gateway for the formation of long-term but not short-term sensorimotor memories, mirroring the role of the MTL for declarative memories. It thus reveals the existence of distinct neural substrates for short-term and long-term sensorimotor memory, and it explains both the trial-to-trial differences identified in this study and long-standing study-to-study differences in the effects of cerebellar damage on sensorimotor learning ability.

Case report: Refractory focal motor seizure associated with cerebrospinal fluid neurochondrin antibody.

Background: Focal onset seizures, characterized by localized neuronal hyperexcitability in the brain, can be related to various structural, immune, genetic, or metabolic abnormalities. Autoimmune epilepsies are increasingly recognized. Neurochondrin antibody has been reported in a variety of rare autoimmune neurological disorders. This article aims to highlight the relevance of anti-neurochondrin in autoimmune epilepsy. Methods: This is a case presentation and literature review of autoimmune epilepsy associated with anti-neurochondrin antibody. Case presentation: A 26-year-old African American right-handed man with a history of Sjogren's syndrome presented with near constant, rhythmic left-sided facial twitching movements, and one episode of generalized tonic clonic seizure. Magnetic resonance imaging (MRI) of the brain revealed borderline low volume right hippocampus. Cerebrospinal fluid (CSF) studies yielded elevated protein and mild lymphocytic pleocytosis. Antibody Prevalence in Epilepsy 2 (APE2) score was 6, and autoimmune workup was initiated. Anti-neurochondrin antibody returned positive in the CSF autoimmune encephalitis panel with a titer of 1:512 (Mayo Clinic TEST ID: ENC2). Seizures remained refractory to anti-seizure medications including divalproex, lacosamide, and oxcarbazepine. Immunotherapy with methylprednisolone and immunoglobulin improved his epileptic seizures. Conclusion: This is the first reported case of refractory autoimmune epilepsy with positive CSF anti-neurochondrin antibody. This study contributes to the body of evidence supporting the role of neurochondrin antibody in epilepsy. Considering autoimmune testing in individuals with seizures having APE2 score > 4 can aid in timely diagnosis of immune-mediated epilepsy and initiation of immunotherapy, which can result in favorable clinical outcomes. Diagnosis of autoimmune epilepsy, in most cases, is based on clinical characteristics, MRI results, and CSF findings. In addition to the traditional antibody panel for autoimmune encephalitis, some novel antibodies, such as anti-neurochondrin, should also be considered.

Development of a novel nomogram for predicting prognosis of North Chinese with autoimmune cerebellar ataxia.

PURPOSE: The aim of this study was to develop a prognostic nomogram which could predict the prognosis of north Chinese patients with autoimmune cerebellar ataxia (ACA) after immunotherapy. METHODS: Patients with an initial diagnosis of ACA who accepted first-line immunotherapy at our hospital from March 2018 to May 2023 were retrospectively reviewed. Modified Rankin Scale (mRS) was used to evaluate neurological outcomes. According to the mRS scores after immunotherapy, patients with ACA were divided into good prognosis group (mRS 0-2) and poor prognosis group (mRS 3-6). The nomogram for poor prognosis of ACA patients were built based on logistic regression analysis. The validation of the prognostic model was evaluated by concordance index (C-index), calibration curves, and decision curve analyses (DCAs). RESULTS: A total of 86 patients with ACA who received immunotherapy at our hospital were included in this study. They were randomly divided into a training cohort (n = 60) and a validation cohort (n = 26) at a ratio of 7:3. Multivariate analyses revealed that that prognostic variables significantly related to the poor prognosis of ACA were age, elevated cerebrospinal fluid (CSF) albumin (ALB) and abnormal magnetic resonance imaging (MRI). The nomogram was constructed based on above 3 factors. The C-index of the nomogram was 0.935 (95% CI: 0.884-0.991) in the training set and 0.933 (95% CI: 0.763-0.994) in the validation set. The calibration plots for the nomogram showed that predictions of risk of poor prognosis were almost consistent with actual observations. The DCAs showed great clinical usefulness of the nomograms. CONCLUSION: We successfully developed a nomogram to predict poor prognosis for ACA patients using risk factors of age, elevated CSF-ALB and abnormal MRI.

Epilepsy with eyelid myoclonia in a patient with ATP1A3-related neurologic disorder.

We report on an 11 year old Polish girl who experienced paroxysmal episodes with decreased consciousness, (hemi)plegia, movement disorders, slurred speech, dysphagia, and abnormal eye movements. An extensive etiological work-up (brain MRI, EEG, EMG, NCS, toxic, metabolic, infectious, and auto-immune screening) was not conclusive. A genetic analysis with whole-exome sequencing demonstrated a de novo heterozygous mutation in the ATP1A3 gene (c.2232C>G, p.Asn744Lys). A 48 h video-EEG monitoring that was conducted in our unit later confirmed the absence of ictal discharge during an episode of hemidystonia, demonstrating its non-epileptic etiology. However, several discharges of generalized spike waves, which were facilitated by intermittent photic stimulation and eyelid closure were recorded, of which a few were associated with eyelid myoclonia. Taken together, these findings are characteristic of epilepsy with eyelid myoclonia. The clinical picture of this patient partially fulfills the diagnostic criteria of relapsing encephalopathy with cerebellar ataxia as well as alternating hemiplegia of childhood. It is increasingly recognized that the distinct syndromes described with ATP1A3 mutations are overlapping and could be identified in the same patients. Certain variations in ATP1A3 have been linked to an increased risk of developing generalized epilepsy syndromes. We hereby present the second case in the literature of a patient with epilepsy with eyelid myoclonia with an ATP1A3-related neurological disorder.

Early-onset phenotype in a patient with an intermediate allele and a large SCA1 expansion: a case report.

BACKGROUND: Spinocerebellar ataxia type 1, is a rare neurodegenerative disorder with autosomal dominant inheritance belonging to the polyglutamine diseases. The diagnosis of this disease requires genetic testing that may also include the search for CAT interruption of the CAG repeat tract. CASE PRESENTATION: One 23-years-old patient suffers from a severe ataxia, with early-onset and rapid progression of the disease. His father might have been affected, but no molecular confirmation has been performed. The genetic results were negative for the Friedreich's ataxia, spinocerebellar ataxia type 2, 3, 6, 7 and 17. The numbers of CAG repeats in the ATXN1 gene was assessed by fluorescent PCR, tripled-primed PCR and enzymatic digestion for the search of sequence interruption in the CAG repeats. The patient carried one pathogenic allele of 61 CAG and one intermediate allele of 37 CAG in the ATXN1 gene. Both alleles were uninterrupted. CONCLUSIONS: We report a rare case of spinocerebellar ataxia type 1 with an intermediate allele and a large SCA1 expansion. The determination of the absence of CAT interruption brought crucial information concerning this molecular diagnosis, the prediction of the disease and had practical consequences for genetic counseling.

Cerebellar ataxia, neuropathy and vestibular areflexia syndrome (CANVAS): a family with five affected sibs from Turkey.

BACKGROUND: Cerebellar ataxia, neuropathy and vestibular areflexia syndrome (CANVAS), a relatively common cause of late-onset progressive ataxia, is a genetic disease characterised by biallelic pentanucleotide AAGGG repeat expansion in intron 2 of the replication factor complex subunit 1 gene. Herein, we describe the first molecularly confirmed CANVAS family with five affected siblings from Turkey. CASE PRESENTATION: The family comprised seven siblings born from healthy non-consanguineous parents. CANVAS phenotype was present in five of them; two were healthy and asymptomatic. Chronic cough was the first symptom reported in all five siblings, followed by the development of sensory symptoms, oscillopsia and imbalance. Clinical head impulse test (HIT) was positive in all cases and video HIT performed on three patients revealed very low vestibulo-ocular reflex gains bilaterally. Magnetic resonance imaging and nerve conduction studies revealed cerebellar atrophy and sensory neuronopathy, respectively. RP-PCR confirmed the homozygous presence of the AAGGG repeat expansion in all five cases. CONCLUSION: Genetic screening for CANVAS should be considered in all patients with late-onset ataxia, sensory disturbances and vestibular involvement, especially in the presence of chronic cough.

Repeat expansion disorders.

An increasing number of repeat expansion disorders have been found to cause both rare and common neurological disease. This is exemplified in recent discoveries of novel repeat expansions underlying a significant proportion of several late-onset neurodegenerative disorders, such as CANVAS (cerebellar ataxia, neuropathy and vestibular areflexia syndrome) and spinocerebellar ataxia type 27B. Most of the 60 described repeat expansion disorders to date are associated with neurological disease, providing substantial challenges for diagnosis, but also opportunities for management in a clinical neurology setting. Commonalities in clinical presentation, overarching diagnostic features and similarities in the approach to genetic testing justify considering these disorders collectively based on their unifying causative mechanism. In this review, we discuss the characteristics and diagnostic challenges of repeat expansion disorders for the neurologist and provide examples to highlight their clinical heterogeneity. With the ready availability of clinical-grade whole-genome sequencing for molecular diagnosis, we discuss the current approaches to testing for repeat expansion disorders and application in clinical practice.

Encephalopathy with cerebellar deficits in a context of hyponatremia.

BACKGROUND: Hyponatremia can present with various neurological manifestations ranging from altered mental status to cerebral herniation and death. However, cerebellar symptomatology has been rarely reported. CASE PRESENTATION: A 53-year-old male with a history of diabetes mellitus type 2, hypothyroidism, and anxiety disorder presented with impaired level of consciousness and ataxia. His laboratory tests were consistent with sepsis (staphylococcus aureus in blood culture), hyponatremia with euvolemia, low serum and high urine osmolarity. Brain computerized tomography revealed diffuse cerebral edema. Antibiotics and sodium replenishment were initiated. A lumbar puncture and subsequent investigations ruled out alternative etiologies (metabolic, autoimmune, paraneoplastic and other infectious causes). Repeated brain magnetic resonance imaging excluded osmotic demyelination syndromes. After serum sodium restoration his symptoms gradually improved. DISCUSSION: We highlight reversible cerebellar ataxia as a rare manifestation of hyponatremia, in the context of sepsis and possible syndrome of inappropriate antidiuretic hormone ADH release. Extensive diagnostic work-up is essential for the exclusion of other diagnoses.

A Novel MAG Variant Causes Hereditary Spastic Paraplegia in a Consanguineous Pakistani Family.

Background and objectives: Hereditary spastic paraplegia (HSP) is characterized by unsteady gait, motor incoordination, speech impairment, abnormal eye movement, progressive spasticity and lower limb weakness. Spastic paraplegia 75 (SPG75) results from a mutation in the gene that encodes myelin associated glycoprotein (MAG). Only a limited number of MAG variants associated with SPG75 in families of European, Middle Eastern, North African, Turkish and Palestinian ancestry have been documented so far. This study aims to provide further insight into the clinical and molecular manifestations of HSP. Methods: Using whole-exome sequencing, we investigated a consanguineous Pakistani family where three individuals presented with clinical signs of HSP. Sanger sequencing was used to carry out segregation analysis on available family members, and a minigene splicing assay was utilized to evaluate the effect of the splicing variant. Results: We identified a novel homozygous pathogenic splice donor variant in MAG (c.46 + 1G > T) associated with SPG75. RNA analysis revealed exon skipping that resulted in the loss of a start codon for ENST00000361922.8 isoform. Affected individuals exhibited variable combinations of nystagmus, developmental delay, cognitive impairments, spasticity, dysarthria, delayed gait and ataxia. The proband displayed a quadrupedal stride, and his siblings experienced frequent falls and ataxic gait as one of the prominent features that have not been previously reported in SPG75. Conclusions: Thus, the present study presents an uncommon manifestation of SPG75, the first from the Pakistani population, and broadens the spectrum of MAG variants.

Lower limb nerve ultrasound: A four-way comparison of acquired and inherited axonopathy, inherited neuronopathy and healthy controls.

INTRODUCTION/AIMS: In a recent study, we showed that nerve ultrasound of the upper limbs could distinguish inherited sensory neuronopathy from inherited axonopathy; surprisingly, no differences were found in the lower limb nerves. In this study, we compared lower limb nerve ultrasound measurements in inherited neuronopathy, inherited axonopathy, and acquired axonopathy. METHODS: Tibial and sural nerve ultrasound cross-sectional areas (CSAs) of 34 healthy controls were retrospectively compared with those of three patient groups: 17 with cerebellar ataxia with neuronopathy and vestibular areflexia syndrome (CANVAS), 18 with Charcot-Marie-Tooth type 2 (CMT2), and 18 with acquired length-dependent sensorimotor axonal neuropathy, using ANOVA with post-hoc Tukey honestly significance difference (HSD) (significance level set at p < .05). RESULTS: The nerve CSAs of CANVAS and CMT2 patients were not significantly different. Both the tibial and the sural nerve CSAs were significantly smaller in CANVAS and CMT2 compared with the acquired axonal neuropathy group. Tibial nerve CSAs of CANVAS and CMT2 were significantly smaller than controls. Tibial and sural nerve CSAs of the acquired axonal neuropathy group were also significantly larger than the controls'. DISCUSSION: Ultrasound of the lower limb nerves distinguished inherited from acquired axonopathy with the nerve size respectively reduced and increased in these two groups. This has potential implication for the differential diagnosis of these diseases in clinical practice.

Multiple system atrophy mimics CASPR2 antibody-associated disease: a case report.

Aim: Multiple system atrophy (MSA) and CASPR2 antibody-associated disease bear their own characteristics.Case presentation: A 58-year-old woman presented with a 26 months history of uncoordinated gait and slurred speech. Her serum was positive for anti-CASPR2 antibodies, and MRI revealed atrophy of the brainstem and cerebellum. She underwent three plasma exchanges (PE) and received high doses of corticosteroids without any apparent effect. Her autonomic dysfunction improved after repetitive transcranial magnetic stimulation. Eventually, a diagnosis of MSA-cerebellar phenotype(MSA-C) was made.Conclusion: With increased availability of tools for neuron antibody detection, physicians need to be aware of the possibility that antibodies may accompany other diseases. This report underscores the modern dilemmas caused by available and extensive neuron antibody testing.

There is a certain degree of difficulty in diagnosis of MSA, especially in the early stage and it is easy to be confused with degenerative diseases such as PD. With a thoroughly study of autoimmune diseases of the nervous system, it was found that the clinical symptoms of CASPR2-associated disease overlapped with MSA. In this report, a 58-year-old woman was reported to have uncoordinated gait and slurred speech, and anti-CASPR2 antibodies were found in the blood and cerebrospinal fluid for multiple times, which brought great challenges to the diagnosis. After immunotherapy, anti-CASPR2 antibodies titers declined, but the clinical symptoms and brainstem and cerebellar atrophy were exacerbated, MSA-C was finally diagnosed and rTMS treatment seems helpful.

Movement disorders in Megalencephalic Leukoencephalopathy with subcortical cysts - A case series.

BACKGROUND: Megalencephalic leukoencephalopathy with subcortical cysts (MLC) has been described in the literature mostly as early-onset leukodystrophy with cerebellar ataxia being the main clinical phenotype. However, other associated movement disorders have also been reported discretely. CASES: Here, we present seven cases of MLC. Cerebellar ataxia was common in them, while dystonia was present in six, parkinsonism in one and stereotypy in two. Six of them, belonging to the Agarwal community, had the common c.135dup variant. CONCLUSION: Our observation highlights the presence of movement disorders in MLC beyond cerebellar ataxia and phenotypic variability of the c.135dup variant, prevalent in the Agarwal community.

Nerve ultrasound in CANVAS-spectrum disease: Reduced nerve size distinguishes genetically confirmed CANVAS from other axonal polyneuropathies.

BACKGROUND AND AIMS: Ultrasound nerve cross-sectional area (CSA) of patients affected with axonal neuropathy usually shows normal value. Cerebellar ataxia, neuropathy and vestibular areflexia syndrome (CANVAS) seems to represent an exception, showing smaller CSA, but previous reports did not test for biallelic RFC1 gene repeat expansions. METHODS: We compared nerve CSA from CANVAS patients (tested positive for biallelic RFC1 gene repeat expansions) with the CSA from a group of patients with chronic idiopathic axonal polyneuropathy (CIAP) who tested negative for RFC1 gene repeat expansions, hereditary axonal neuropathy (Charcot-Marie-Tooth type 2, CMT2), and Friedreich ataxia (FRDA). RESULTS: We enrolled 15 CANVAS patients (eight men, mean age 66.3 ± 11.5 years, mean disease duration 9.3 ± 4.1 years), affected with sensory axonal neuronopathy. Controls consisted of 13 CIAP (mean age 68.5 ± 12.8 years, seven men), seven CMT2 (mean age 47.9 ± 18.1 years, four men), 12 FRDA (mean age 33.7 ± 8.8, five men). Nerve ultrasound was performed at median, ulnar, sciatic, sural, and tibial nerves and brachial plexus, bilaterally. The nerve CSA from CANVAS patients was significantly smaller than the one from the other cohorts at several sites with significant and high accuracy at Receiver-operating characteristic (ROC) curve analyses. RFC1 AAGGG pentanucleotide expansion, disease duration, and disability did not correlate with CSA at any site, after Bonferroni correction. INTERPRETATION: Decreased sonographic nerve sizes, in arms and legs, in patients with sensory neuropathy and normal motor conduction studies could point to CANVAS-spectrum disease and help guide appropriate genetic testing.

Effects of Non-Invasive Brain Stimulation for Degenerative Cerebellar Ataxia: A Systematic Review and Meta-Analysis.

BACKGROUND: This systematic review and meta-analysis aimed to assess the effectiveness of non-invasive brain stimulation (NIBS), including repetitive transcranial magnetic stimulation (rTMS) and transcranial electrical stimulation (tES), as a neurological intervention for degenerative cerebellar ataxia (DCA) based on preregistration (PROSPERO: CRD42023379192). OBJECTIVE: We aimed to explore clinical outcomes and examine the parameters associated with NIBS efficacy in DCA patients. METHODS: The PubMed, Cochrane Library, CHINAL, and PEDro databases were searched for relevant randomized controlled trials (RCTs). Data extraction, quality assessment, and heterogeneity analyses were conducted; the Grading, Recommendations, Assessment, Development, and Evaluation was used to assess the quality of evidence and a meta-analysis was performed. RESULTS: Seventeen RCTs that included 661 patients on the scale for assessment and rating of ataxia (SARA) and 606 patients on the International Cooperative Ataxia Rating Scale (ICARS) were included. These RCTs showed a serious risk of bias (RoB) and low certainty of evidence for both outcomes. NIBS significantly reduced SARA (MD = -2.49, [95% confidence interval: -3.34, -1.64]) and ICARS (-5.27 [-7.06, -3.47]); the subgroup analysis showed significant effects: rTMS and tES reduced both outcomes. However, there were no significant differences in the effects of rTMS and tES. Additional subgroup analysis indicated the impact of rTMS frequency and the total number of tES sessions on ataxia. CONCLUSION: Non-invasive brain stimulation may reduce ataxia in DCA patients, but the estimated effect size may change in future studies because the RoB was serious and the certainty of evidence was low, and the heterogeneity was high. To establish evidence for selecting NIBS methods and parameters, continued high-quality RCTs are required.

Acute Cerebellar Manifestations without Limbic Involvement in GABAB Receptor Autoimmune Encephalitis: Case Report and Literature Review.

Autoimmune encephalitis is a rapidly progressive inflammatory brain disease. Gamma-aminobutyric acid type B (GABAB) receptor autoimmune encephalitis is a rare subtype characterized by distinct clinical features. Diagnosis can be especially challenging when typical limbic symptoms and neuroimaging findings are absent. This case report underscores the importance of identifying this condition and starting immunosuppressive treatment promptly. A 59-year-old man presented with gait disturbances, dysarthria, and severe ataxia without cognitive impairment. Initial examinations, including a brain MRI, were unremarkable, except for an elevated cell count and protein in the cerebrospinal fluid. Despite receiving initial empirical antiviral treatment, his symptoms worsened, prompting the administration of intravenous methylprednisolone and immunoglobulin. After these immunosuppressive therapies, the cerebellar symptoms showed gradual improvement. Subsequent testing for antibodies to the GABAB receptor was positive in both the serum and cerebrospinal fluid. Follow-up MRI revealed cerebellar atrophy, consistent with a diagnosis of GABAB receptor-associated acute cerebellitis. This case illustrates that cerebellar symptoms can occur in the absence of more common limbic manifestations in GABAB receptor autoimmune encephalitis. The progression of cerebellar atrophy following an initially normal MRI is a significant finding that offers supporting evidence for the diagnosis of cerebellitis. A review of the literature identified similar cases of acute cerebellitis without limbic symptoms, although neuroimaging abnormalities in the cerebellum were not reported. Our case underscores the importance of increased clinical awareness and consideration of autoimmune causes, even when neuroimaging appears normal. Early and appropriate immunosuppressive therapy may help change the course of the disease and enhance patient outcomes.

Comprehensive Physiotherapy Rehabilitation in a Patient With Cerebellar Ataxia and Dysphagia: A Case Report Investigating Symptomatology, Management, and Outcomes.

A cerebellar infarct occurs when blood flow to the cerebellum, located in the posterior cranial fossa, is disrupted. This diminished blood supply leads to decreased oxygen delivery, resulting in motor and balance control impairments. One prevalent sign of neurodegenerative diseases is dysphagia, which is typically linked to a higher death rate. No systematic and uniform assessment of dysphagia is used in the clinical care environment of individuals with ataxia. Its effect on the quality of life associated with health in patients is little understood. Therefore, this case report works to address dysphagia in cerebellar ataxia. This case report examines the physiotherapy management of a 41-year-old male who had cerebellar ataxia secondary to an infarct in the bilateral cerebellar hemisphere and vermis. The rehabilitation period lasted for six weeks. On examination, the patient had difficulty swallowing and showed symptoms of cerebellar dysfunctions, such as nystagmus, dyssynergia, dysmetria, and dysdiadochokinesia. Neuro-physiotherapy interventions, like conventional physiotherapy, trunk, and pelvis proprioceptive neuromuscular facilitation (PNF), Kinesio taping for dysphagia, interventions to treat gait, balance training interventions, and Frenkel's exercises were commenced. The outcome measures were evaluated using standardized outcome measures like the Swallowing Quality of Life Scale (SWAL-QOL), Severity of Ataxia Scale (SARA), Trunk Impairment Scale (TIS), Berg Balance Scale (BBS), Barthel Index, and World Health Organization Quality of Life (WHO-QOL). We conclude that a properly structured physiotherapy program subsequently improved the symptoms of patients. Furthermore, it enhanced functional independence, which subsequently improved the patient's quality of life.

Neurological Complications of COVID-19 Infection: A Comprehensive Review.

The COVID-19 pandemic is well on its way to reaching endemic status across the globe. While the medical community's understanding of the respiratory complications induced by COVID-19 is improving, there is still much to be learned about the neurological manifestations associated with COVID-19 infection. This review aimed to compile relevant, available evidence of COVID-19-induced neurological complications and to provide information for each complication regarding symptomology, progression patterns, demographic risk factors, treatment, and causative mechanism of action when available. Data for this review was collected using a confined search on PubMed using the keywords ["COVID-19" OR "SARS-CoV-2"] AND ["neurological complications" OR "olfactory symptoms" OR "gustatory symptoms" OR "myalgia" OR "headache" OR "dizziness" OR "stroke" OR "seizures" OR "meningoencephalitis" OR "cerebellar ataxia" OR "acute myelitis" OR "Guillain Barré Syndrome" OR "Miller Fisher Syndrome" OR "Posterior Reversible Encephalopathy Syndrome"] between 2019 and 2023. A wide range of neurological manifestations impact a significant percentage of COVID-19 patients, and a deeper understanding of these manifestations is necessary to ensure adequate management. The most common neurological complications identified consist of olfactory and gustatory dysfunctions, myalgia, headache, and dizziness, while the most severe complications include stroke, seizures, meningoencephalitis, Guillain-Barré syndrome, Miller Fisher syndrome, acute myelitis, and posterior reversible encephalopathy syndrome. While this review effectively provides a roadmap of the neurological risks posed to COVID-19 patients, further research is needed to clarify the precise incidence of these complications and to elucidate the mechanisms responsible for their manifestation.