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This letter presents a case study of a 34-year-old man with relapsing-remitting multiple sclerosis (RRMS) who developed severe progressive multifocal leucoencephalopathy (PML) after using natalizumab. The patient was treated with various interventions, including plasmapheresis and intravenous immunoglobulin, but did not show clinical improvement. However, after receiving pembrolizumab, the patient experienced significant clinical improvement, including improved mobility and cognitive function. The use of pembrolizumab in PML associated with natalizumab is a novel approach, and more research is needed to determine its effectiveness in similar cases. [Extracted from the article]

Tumor necrosis factor-alpha inhibitors and immune-checkpoint inhibitors are the most frequently reported agents, but recently, the number of cases reporting iatrogenic central nerve demyelination with tyrosine kinase inhibitors has increased. Tumor necrosis factor-alpha inhibitors and immune-checkpoint inhibitors are the most frequently reported agents in iatrogenic central nervous system demyelination cases [[1]]. As treatment options for cancer and autoimmune diseases are developing each day, iatrogenic central demyelination case reports are increasing in number. [Extracted from the article]

This document is a letter to the editor discussing a case study of a 32-year-old female patient with psoriasis and multiple sclerosis who developed both generalized and patch granuloma annulare after treatment with fingolimod. Granuloma annulare is an inflammatory cutaneous disorder that can present in various forms and has been associated with diabetes, hyperlipidemia, malignancy, infections, and certain medications. The patient in this case had a family history of psoriasis and was treated with topical medications before starting fingolimod. The authors suggest that T lymphocytes may play a role in the development of fingolimod-induced granuloma annulare, and this case contributes to the literature on this rare topic. [Extracted from the article]

Progressive multifocal leukoencephalopathy (PML) is a severe demyelinating disease of the central nervous system caused by reactivation of the polyomavirus JC (JCV). Human immunodeficiency virus (HIV) infection is one of the leading causes of PML which has high morbidity and mortality due to the lack of a proven standard treatment. We found clinical and radiological improvement with the combination of high-dose methylprednisolone, mirtazapine, mefloquine, and IVIG in our patient who presented with neurological symptoms and had diagnosed concurrent acquired immunodeficiency syndrome (AIDS) and PML. To our knowledge, our case is the first HIV-associated PML which responded to this combination therapy. [ABSTRACT FROM AUTHOR]

We aimed to assess the visual fields and optical coherence tomography (OCT) measurements in patients with multiple sclerosis (MS) to detect subclinical visual system disease. The study included 15 MS patients with previous optic neuritis (Group I), 17 MS patients without previous optic neuritis (Group II), and 14 healthy controls (Group III). Each subject underwent standard automated perimetry (SAP), frequency doubling technology perimetry (FDTP), and OCT. The mean deviation of SAP in Group I was lower than those in Groups II (p =.018) and III (p =.001). The pattern standard deviation of SAP in Group I was higher than those in Group III (p <.0001). The mean deviation of FDTP in Groups I and II was lower than those in Group III (p =.0001 and p =.016, respectively). The temporal quadrant of the retinal nerve fibre layer in Group I was thinner than those in Groups II and III (p =.005 and p =.003, respectively). The mean macular volume in Group I was thinner than those in Groups II and III (p =.004 and p =.002, respectively). A single method is inadequate for establishing early and/or mild visual impairment in MS. All conventional and non-conventional techniques are complementary in demonstrating subclinical visual damage in MS. [ABSTRACT FROM AUTHOR]

Useless Hand Syndrome (UHS) is a rare clinical manifestation of an upper cervical cord lesion, which is most commonly associated with multiple sclerosis (MS). The pathophysiological mechanism underlying UHS remains unclear. We report a 25-year-old woman, who described numbness in her left upper extremity. Cervical magnetic resonance imaging revealed a posterior upper cervical cord lesion. There was no cortical lesion that could explain the clinical findings. We measured (1) short-latency afferent inhibition (SAI) by obtaining motor evoked potentials as an indicator of sensorimotor integration and (2) somatosensorial temporal discrimination threshold (STDT) to display central somatosensory pathway function. In the right cerebral hemisphere, we found an excessive increase in STDT and no inhibition in the SAI paradigm. These findings indicate that impairment of sensorimotor integration and central processing of sensory stimuli cause useless hand syndrome. [ABSTRACT FROM AUTHOR]

Spinal, general, and epidural anesthesia have been implicated in the exacerbation of multiple sclerosis. However, to date, no attack has been reported following usage of mandibular block articaine anesthesia. This article describes the case of a 30-year-old man who presented with a sudden occurrence of diplopia on lateral gaze the day after extraction of the mandibular right second and third molars. Two times 1.8 mL 4% articaine solution with 1/100,000 adrenaline was used for local anesthesia. On neurological examination, a restriction on external gaze of his left eye was observed. Immunoglobulin G index was high, and oligoclonal band was present in spinal fluid evaluation. MRI revealed demyelinated plaques on the left side of the midpons, right cerebellar hemisphere, and bilateral white matter and supraventricular spaces. The left abducens palsy completely improved after treatment with intravenous methylprednisolone. Mandibular block articaine anesthesia may precipitate multiple sclerosis onset or attack. This case indicates that dental clinicians and neurologists may be alerted to isolated abducens palsy as a possible adverse effect of mandibular block articaine anesthesia. [ABSTRACT FROM AUTHOR]

The prevalence of pathological laughing and crying in multiple sclerosis (MS) is 10%. It has been speculated that the anatomical lesion responsible for the pathological laughing is located in the pontine base, prefrontal cortex, and cerebellum. We report an 18-year-old male patient presenting with pathological laughing and hypomania. In his neurological examination, he had a euphoric effect with ataxic walking and dysarthria speech. He had a bilateral conjugated gaze limitation, with a prominent bilateral horizontal nystagmus on left gaze, dysmetria, dysdiadokokinesia, and remarkable dysfunction in a heel-to-shin test on the left. The IgG index in cerebrospinal fluid was normal with an oligoclonal band was present. In cranial MRI, there was a lesion on central pons which was hypointense in T1 images with contrast enhancement and hyperintense in T2 and flair images. Also another lesion in right brachium pontis which did not contrast enhancement but was hyperintense on T2 and flair images was present. There was an elevation of myoinositol/creatine ratio and choline and a reduction of NAA in proton MR spectroscopy. MR spectroscopic evaluation of the patient demonstrated the demyelination process. There has been no report of patients in whom pathological laughter was the presenting symptom of clinically isolated brainstem syndrome. [ABSTRACT FROM AUTHOR]

This study investigated the presence of sub-clinical cognitive dysfunction in patients with clinically isolated syndrome (CIS) and the abnormalities of cognitive event-related potentials (ERPs). Subclinical cognitive dysfunction was assessed in 20 patients with CIS and in 20 healthy controls. Patients had impairments in verbal learning and long-term memory, evaluating attention, executive function and visuospatial skills, in decreasing order of frequency. SDLT and SIT were the most, and COWAT and BNT were the least affected tests. The N200 and P200 latencies were prolonged, and N100, N200 and P200 amplitudes were reduced in the patients relative to the controls, from the Fz, Cz and Pz electrode positions ( p<0.05). Detailed cognitive testing is valuable in determining subclinical cognitive dysfunction in CIS patients. ERP abnormalities as well as abnormalities in detailed cognitivetesting in patients with CIS are helpful in the diagnosis of sub-clinical cognitive dysfunction. [ABSTRACT FROM AUTHOR]

Marchiafava-Bignami disease (MBD) is characterized by demyelination and necrosis of corpus callosum encountered in chronic alcoholic patients. Etiology is the deficiency of vitamin B complex. Magnetic resonance imaging (MRI) in MBD typically reveals focal lesions of high T2 and FLAIR signal intensity in the corpus callosum. We here present a 42-year-old male alcoholic diagnosed as MBD on the basis of MRI and diffusion-weighted imaging (DWI) features. The patient totally recovered following appropriate vitamin B complex replacement therapy, despite reduced diffusion in the initial setting. This case report emphasizes on the important role played by MRI and DWI in the early diagnosis and follow-up of this potentially fatal disease. [ABSTRACT FROM AUTHOR]