BACKGROUND: CHANTER (Cerebellar Hippocampal and Basal Nuclei Transient Edema with Restricted diffusion) is a recently described syndrome occurring in the context of drug abuse. While clinical findings are rather unspecific (disorientation, unresponsiveness), MR imaging (MRI) discloses a characteristic pattern (restricted diffusion in the basal ganglia and hippocampi, cerebellar oedema and haemorrhage), allowing for timely diagnosis before complications such as cerebellar swelling and herniation do occur. Here we report a case of CHANTER primarily based on imaging findings, as there was no evidence of drug abuse on admission.
METHODS: A 62-year-old Patient was admitted to our hospital after being unresponsive at home. Prehospital intubation was performed, which limited neurological assessment. Under these circumstances no obvious symptoms could be determined, i.e. pupils were isocoric and responsive, and there were no signs of seizures. While the initial CT scan was unremarkable, the subsequent MRI scan showed a distinct imaging pattern: moderately enhancing areas in the basal ganglia and hippocampi with diffusion restriction, accompanied by cerebellar haemorrhage and oedema (Figs. 1 and 2). A comprehensive clinical and laboratory work-up was performed, including drug screening, spinal tap, Holter ECG, echocardiography and EEG. The only conspicuous anamnestic finding was a chronic pain syndrome whose medication had been supplemented with opioids two months previously. The opioid medication was discontinued, which led to a rapid improvement in the patient\'s clinical condition without any further measures. The patient was able to leave the intensive care unit and was discharged 10 days after admission without persistent neurological deficits.
CONCLUSIONS: Familiarity with typical MRI patterns of toxic encephalopathy in patients from high-risk groups, such as drug abusers, is crucial in emergency neuroradiology. In the presence of typical MRI findings, CHANTER syndrome should be included in the differential diagnosis, even if there is no history of drug abuse, to avoid delay in diagnosis and treatment.

Huntington\'s disease (HD), referred to as Huntington\'s chorea, is an infrequent neurodegenerative ailment with an autosomal-dominant inheritance pattern characterized by the progressive deterioration of GABAergic neurons in the basal ganglia. Other ones include subcortical-type dementia, behavioral abnormalities, midlife psychosis, and gradual inadvertent choreoathetosis movements. HD is characterized by atrophy of the dorsal striatum (caudate nucleus and putamen) with concurrent expansion of the frontal horns of the lateral ventricles on imaging modalities such as computed tomography (CT) and magnetic resonance imaging (MRI). A molecular study validates the diagnosis of HD by identifying the disorder\'s hallmark amplified CAG triplet. Currently, there is no cure for HD, and treatment focuses on providing supportive care and managing the symptoms. Multidisciplinary approaches involving healthcare professionals, neurologists, and psychiatrists are crucial for comprehensive management. Medications are used to alleviate motor symptoms and manage psychiatric manifestations. Physical and occupational therapies help maintain functional abilities and improve quality of life. Genetic counseling and psychosocial support are essential for patients and their families. An additional crucial objective entails advancing more precise and dependable techniques for the timely identification and assessment of HD. Timely interventions and improved symptom management are made possible by early diagnosis. Based on clinical and imaging findings, we present a case of HD in a 62-year-old female.

We systematically reviewed case reports of posterior reversible encephalopathy syndrome (PRES), and investigated the characteristics of PRES in pregnant Japanese women and the clinical relevance of reversible cerebral vasoconstriction syndrome (RCVS) in pregnant women with PRES. Articles were collected using the PubMed/Medline and Ichushi-Web databases. This review was ultimately conducted on 121 articles (162 patients). The clinical characteristics of PRES, individual sites of PRES lesions, edema types, and clinical characteristics of RCVS in PRES cases were examined. The most common individual site of PRES lesion was the occipital lobe (83.3%), followed by the basal ganglia, parietal lobe, frontal lobe, brain stem, cerebellum, temporal lobe, thalamus, and splenium corpus callosum (47.5, 42.6, 24.7, 16.1, 9.3, 5.6, 4.3, and 0.0%, respectively). Edema types in 79 cases with PRES were mainly the vasogenic edema type (91.1%), with very few cases of the cytotoxic edema type (3.8%) and mixed type (5.1%). Among 25 PRES cases with RCVS, RCVS was not strongly suspected in 17 (68.0%) before magnetic resonance angiography. RCVS was observed at the same time as PRES in 13 cases (approximately 50%), and between days 1 and 14 after the onset of PRES in the other 12. These results suggest that the basal ganglia is a frequent site of PRES lesions in pregnant women. RCVS may occur at or after the onset of PRES, even if there are no symptoms to suggest RCVS.

Pain is a common symptom in multiple sclerosis (MS), especially neuropathic pain, which has a significant impact on patients\' mental and physical health and quality of life. However, risk factors that related to neuropathic pain, still remain unclear.
The study aimed to explore the risk factors of neuropathic pain among MS patients.
This retrospective study examined the consecutive patients diagnosed with MS in the Department of Neurology of Guangdong Provincial Hospital of Chinese Medicine between August 2011 and October 2022. Neuropathic pain was defined as \"pain arising as a direct consequence of a lesion or disease affecting the somatosensory system\". Demographic and clinical features were obtained from the electronic system of the hospital.
Our cohort revealed that the prevalence of patients with neuropathic pain in MS was 34.1%. The results indicated that the longer the spinal lesions, the greater the neuropathic pain risks (2-4: OR, 13.3(2.1-82), >5: OR, 15.2(2.7-86.8), p for tread: 0.037). Meanwhile, multivariate regression analysis showed that cervical and thoracic lesions (OR 4.276, 95% CI 1.366-13.382, P = 0.013), upper thoracic lesions (T1-T6) (OR 3.047, 95% CI 1.018-9.124, P = 0.046) were positively correlated with neuropathic pain, while basal ganglia lesions (OR 0.188, 95% CI 0.044-0.809, P = 0.025) were negatively correlated with neuropathic pain among MS patients.
Extended spinal lesions (≥3 spinal lesions), cervical and thoracic lesions, upper thoracic lesions were independent risk factors of neuropathic pain among MS patients. Furthermore, our study found that the longer the spinal lesions, the greater the neuropathic pain risks.

Nitrous oxide abuse may cause functional cobalamin deficiency and subsequent damage to the peripheral nerves, the spinal cord, and the brain, a symptom complex best described by the term cobalamin neuropathy. Here, we report a case of cobalamin neuropathy with uncommon cerebral symptomatology following nitrous oxide intoxication and contextualize the symptomatology. A 22-year-old male with a history of mixed drug dependency presented at the emergency room after inhaling six 615 g cylinders, equal to ~1800 L, of nitrous oxide daily for two weeks. His main complaints were rapidly progressing paresthesias and gait difficulties, but he was also found to suffer from memory impairment and signs of extrapyramidal pathology in the form of dystonic posturing and athetosis. Neuroimaging demonstrated spinal cord hyperintensities consistent with subacute combined degeneration. The patient had low serum cobalamin and high plasma homocysteine, suggesting cobalamin neuropathy. After commencing treatment with parenteral hydroxocobalamin, plasma homocysteine normalized. The extrapyramidal symptoms disappeared during the first days of treatment, whereas the cognitive and peripheral symptoms only partially resolved over the following 20 days. This case highlights how neurological symptoms such as hyperkinetic movements and memory impairment may be associated with chronic nitrous oxide abuse. It is unclear to what extent these and other symptoms of cobalamin neuropathy are reversible, which underscores the public health concern.

Idiopathic basal ganglia calcification (IBGC), also known as Fahr\'s disease, is a rare neurological disorder characterized by metabolic, biochemical, neuroradiological, and neuropsychiatric alterations resulting from symmetrical and bilateral intracranial calcifications. In most cases, an autosomal dominant pattern of inheritance and genetic heterogeneity is observed. Neuropsychiatric symptoms with movement disorders account for 55% of the manifestations of this disease. In this report, we present the case of a 42-year-old Pakistani male who presented to the emergency department with a sudden onset of generalized tonic muscle contractions. His medical history revealed progressive cognitive impairment, and he had a history of taking oral calcium supplements. Initial laboratory investigations showed hypocalcemia with normal magnesium and phosphate levels, while his parathyroid hormone levels were low. The interictal electroencephalogram was normal, and CT imaging of the brain without contrast revealed bilateral symmetrical dense calcifications in the basal ganglia, thalami, periventricular area, corona radiata, centrum semiovale, and dentate nucleus of the cerebellum, suggestive of Fahr disease. Intravenous calcium gluconate was administered in the emergency department, leading to an improvement in the patient\'s symptoms. The diagnosis of IBGC with relevant symptoms was confirmed through laboratory values and characteristic features observed in the CT examination.

UNASSIGNED: Quantitative susceptibility mapping (QSM) is a magnetic resonance imaging (MRI) technique that can measure the magnetic susceptibility of tissues, which can reflect their iron content. QSM has been used to detect iron accumulation in cortical and subcortical brain regions. However, its application in subcortical regions such as the basal ganglia, particularly the putamen, is rare in patients with amyotrophic lateral sclerosis (ALS).
UNASSIGNED: We present the case of a 40-year-old male patient with ALS who underwent an MRI for QSM. We compared his QSM images with those of a control subject and performed a quantitative analysis of the magnetic susceptibility values in the putamen regions. We also reviewed the literature on previous QSM studies in ALS and summarized their methods and findings. Our QSM analysis revealed increased magnetic susceptibility values in the bilateral putamen of the ALS patient compared to controls, indicating iron overload. This finding is consistent with previous studies reporting iron dysregulation in subcortical nuclei in ALS. We also discussed the QSM processing techniques used in our study and in the literature, highlighting their advantages and limitations.
UNASSIGNED: This case report demonstrates the potential of QSM as a sensitive MRI biomarker for evaluating iron levels in subcortical regions of ALS patients. QSM can provide quantitative information on iron deposition patterns in both motor and extra-motor areas of ALS patients, which may help understand the pathophysiology of ALS and monitor disease progression. Further studies with larger samples are needed to validate these results and explore the clinical implications of QSM in ALS.

Hypoglycemia is known as a sudden diminution in blood glucose level <50 mg/dL. Hypoglycemic encephalopathy is a metabolic encephalopathy that is usually observed in patients treated for diabetes or chronic alcoholism. Neurological manifestations may range from transient deficits to prolonged coma, depending on the duration and severity of hypoglycemia. Neuroradiological features of hypoglycemia are variable involving the cerebral white and gray matter regions. Acquired metabolic or toxic conditions can cause hypoglycemia-like damage to the cerebral white matter and basal ganglia. Widespread lesions in the brain parenchyma or basal ganglia have a poor prognosis. In this report, we present a patient with widespread brain damage secondary to profound and prolonged hypoglycemia.

OBJECTIVE: Major neurocognitive Disorder (NCD) is a largely heterogeneous condition with numerous etiological possibilities. Most diagnosed cases have unspecified origins. As such, Fahr\'s syndrome (FS) is a rare neurodegenerative condition that clinically presents with varying neurologic, neuropsychiatric, and movement disorder features. FS is characterized by bilateral basal ganglia calcifications secondary to other conditions (e.g., endocrine and metabolic disorders, infectious diseases). This case will expand upon the literature of rare and poly-etiological presentations of NCD.
METHODS: A 75-year-old White male underwent neuropsychological evaluation due to concerns from his wife regarding sudden onset of diminished mood, anhedonia, hypersomnia, disinhibition, and idiosyncratic motor movements two years prior which worsened after contracting COVID-19. Patient has multiple co-morbid medical conditions including hypothyroidism, hypercholesterolemia, intermediate hyperglycemia, prostate cancer (in remission), and history of a syncopal episode. Neuroimaging was remarkable for bilateral basal ganglia calcifications and white matter lesions.
RESULTS: At the exam, patient exhibited hypomimia, ataxic gait, alogia, sporadic motor stereotypies, and motor overflow. Overall performance on the Meyers Neuropsychological Battery was Below Average with relative weaknesses in attention, memory, processing speed, mental flexibility, and motor functioning. Patient was diagnosed with Major NCD of unspecified etiology and instructed to continue consultation with neurology.
CONCLUSIONS: This patient\'s cognitive difficulties appeared poly-etiological and are likely attributed to the combination of basal ganglia calcification, white matter changes, hypothyroidism, and COVID-19 which suggests the presence of FS. This case exemplifies the importance of considering multiple etiologies, including the implications of COVID-19 during the diagnostic process as more neurologic symptoms of COVID-19 are still being discovered.

Fahr\'s syndrome is defined by the presence of striato-pallido-dentate calcifications. It is a rare entity with clinical polymorphism, and it occurs in patients with dysparathyroidism, especially those with hypoparathyroidism. It must be distinguished from Fahr\'s disease (FD), which is defined by the presence of intracerebral calcifications without phosphocalcic metabolism abnormality. In this paper, we report the particulars of five patients diagnosed with Fahr\'s syndrome revealed by neurological and cognitive disorders, seizures, and abnormal movements associated with tetany crisis. In all cases, brain imaging and biological examinations led to the diagnosis of Fahr\'s syndrome related to hypoparathyroidism. The evolution was favorable after treatment. Fahr\'s syndrome is a rare and serious condition for which treatment is simple and effective. Our observations shed light on the necessity of evaluating phosphocalcic metabolism and exploring cerebral calcifications in patients with neurological disorders.