Prediction and Visualization of Non-Enhancing Tumor in Glioblastoma via T1w/T2w-Ratio Map

One of the challenges in glioblastoma (GBM) imaging is to visualize non-enhancing tumor (NET) lesions. The ratio of T1- and T2-weighted images (rT1/T2) is reported as a helpful imaging surrogate of microstructures of the brain. This research study investigated the possibility of using rT1/T2 as a surrogate for the T1- and T2-relaxation time of GBM to visualize NET effectively. The data of thirty-four histologically confirmed GBM patients whose T1-, T2- and contrast-enhanced T1-weighted MRI and 11C-methionine positron emission tomography (Met-PET) were available were collected for analysis. Two of them also underwent MR relaxometry with rT1/T2 reconstructed for all cases. Met-PET was used as ground truth with T2-FLAIR hyperintense lesion, with >1.5 in tumor-to-normal tissue ratio being NET. rT1/T2 values were compared with MR relaxometry and Met-PET. rT1/T2 values significantly correlated with both T1- and T2-relaxation times in a logarithmic manner (p < 0.05 for both cases). The distributions of rT1/T2 from Met-PET high and low T2-FLAIR hyperintense lesions were different and a novel metric named Likeliness of Methionine PET high (LMPH) deriving from rT1/T2 was statistically significant for detecting Met-PET high T2-FLAIR hyperintense lesions (mean AUC = 0.556 ± 0.117; p = 0.01). In conclusion, this research study supported the hypothesis that rT1/T2 could be a promising imaging marker for NET identification.

Leber’s Hereditary Optic Neuropathy Plus Causing Recurrent Myelopathy due to an MT-DN1 Mutation at G3635A

A 51-year-old man with known Leber’s hereditary optic neuropathy (LHON) presented with worsening lower extremity weakness and numbness. Following an episode of myelopathy two years before, he had been ambulating with a walker but over two weeks became wheelchair bound. He also developed a sensory level below the T4 dermatome to light touch, pinprick, and vibration. MRI of his cervical and thoracic spine showed a nonenhancing T2 hyperintense lesion extending from C2 to T12. At his presentation two years earlier, he was found to have a longitudinally extensive myelopathy attributed to his LHON. Genetic testing revealed a 3635 guanine to adenine mutation. MRI at that presentation demonstrated a C1-T10 lesion involving the central and posterior cord but, unlike the new lesion, did not involve the ventral and lateral horns. Given the similarity to his prior presentation and a negative evaluation for alternative etiologies, he was thought to have recurrent myelopathy secondary to Leber’s Plus. To our knowledge, recurrent myelopathy due specifically to the G3635A mutation in Leber’s Plus has not been reported previously.

A case study: Multiple Lacunar Infarct using Magnetic Resonance Imaging

Background: An ischemic stroke takes place when a blood vessel supplying the brain is blocked and blood circulation to a part of the brain is damaged. A lacunar stroke occurs due to one of the arteries that provide blood to the brain's deep structures is blocked. Case Study: A 55-year-old male patient have right cerebrovascular accident (CVA) with left hemiparesis on 16th of August 2019. Normal result was seen by brain Computed Tomography (CT) scanning. Magnetic Resonance Imaging (MRI) brain was done resulted in hyperintense lesion in right pons and foci and Magnetic Resonance Angiography (MRA) was done and resulted in severe basilar artery stenosis.

Clinical Reasoning: A 57-Year-Old Man With Stepwise Progressive Paraparesis, Sensory Loss, Urinary Retention, and Constipation

We present the case of a 57-year-old man with protein S deficiency and left leg deep vein thrombosis (DVT) five years prior, who developed stepwise progressive bilateral lower limb weakness, numbness/paresthesia, gait imbalance, hesitancy of micturition, and constipation in the setting of recurrent left common femoral DVT treated with apixaban. Symptoms amplified with Valsalva, corticosteroids, and post-lumbar puncture, with longitudinally extensive mid-thoracic T2-hyperintense lesion extending to the conus associated with hazy holocord enhancement on magnetic resonance imaging (MRI), raising suspicion for spinal dural arteriovenous fistula (sDAVF). Initial digital subtraction angiography (DSA) was negative for sDAVF. However, cerebral spinal fluid (CSF) was herpes simplex virus (HSV)-2 positive, and he was treated with antiviral therapy. Unfortunately, he continued to worsen despite treatment. Repeat neuroimaging twelve months after initial presentation demonstrated persistent lower thoracic/conus lesion in addition to cauda equina enhancement and subtle dorsal T2-hypointense flow voids. We raised red flags (eg, lack of clinical prodrome, no herpetic rash, no CSF pleocytosis, and rostral extent of the lesion) that suggested the HSV2 nucleic acid detection was perhaps unrelated to the neurological syndrome. Given the high index of suspicion for sDAVF, we repeated spinal vascular imaging. Spinal MRA demonstrated dilated right dorsal perimedullary veins from T10 to T11. Repeat DSA revealed a right T10 sDAVF. Microsurgical treatment rather than embolization of the fistula was successful without complication, with significant improvement in motor, sphincter, and to a lesser extent sensory function, with residual gait imbalance after inpatient rehabilitation three weeks postoperatively.

Tacrolimus-induced neurotoxicity from bipolar disorder to status epilepticus under the therapeutic serum level: a case report

Background Tacrolimus is a macrolide immunosuppressant widely used to prevent rejection after solid organ transplantation. In general, adverse events of tacrolimus occur more often as the concentration of tacrolimus in the blood increases. We report the case of a 39-year-old man who developed a variety of adverse events despite in the therapeutic level of tacrolimus in the blood. Case presentation A 39-year-old man underwent liver transplantation for liver cirrhosis due to alcoholic liver disease. The postoperative immunosuppressant consisted of tacrolimus (5 mg) and mycophenolate (500 mg) twice daily. Five months after taking tacrolimus, he presented with talkativeness, which gradually worsened. Brain magnetic resonance imaging performed 10 months after tacrolimus administration revealed a hyperintense lesion affecting the middle of the pontine tegmentum on T2WI. The blood concentration of tacrolimus was 7.2 ng/mL (therapeutic range 5–20 ng/mL). After 21 months, he exhibited postural tremor in both the hands. Twenty-four months after taking tacrolimus, he showed drowsy mentality, intention tremor, and dysdiadochokinesia. Electroencephalography presented generalized high-voltage rhythmic delta waves; therefore, tacrolimus was discontinued in suspicion of tacrolimus-induced neurotoxicity, and anticonvulsive treatment was started. The level of consciousness gradually improved, and the patient was able to walk independently with mild ataxia. Conclusion This case shows that tacrolimus-induced neurotoxicity can occur even at normal concentrations. Therefore, if a patient taking tacrolimus exhibits psychiatric or neurologic symptoms, neurotoxicity should be considered even when the blood tacrolimus is within the therapeutic range.

A Septuagenarian With Progressive Hemiparesis

A 78-year-old man with no pertinent medical history sought care for an 18-month history of progressive right lower extremity weakness, gait impairment, and falls. On neurologic examination, he had a hemiparetic gait. He had normal higher cognitive function and cranial nerve function. Motor examination showed decreased bulk over the right hand with no fasciculations, mild spasticity over the right leg, and right hemiparesis with an upper motor neuron pattern. Deep tendon reflexes were brisk throughout his limbs, and he had an extensor plantar reflex on the right side. He had impaired vibratory sense at the toes, with otherwise normal sensory and coordination examinations. Magnetic resonance imaging (MRI) of the brain showed ovoid periventricular and punctate subcortical and deep white matter T2 hyperintense foci. Some of these had corresponding T1 hypointensity. MRI of the cervical spine showed 1 eccentrically located T2 hyperintense lesion over the right lateral aspect of C2. Cerebrospinal fluid analysis showed no pleocytosis, an increased protein concentration of 66 mg/dL, and 4 unique oligoclonal bands. A diagnosis of primary progressive multiple sclerosis, very late onset, was made. With any diagnosis of late-onset multiple sclerosis, a decision about whether multiple sclerosis disease-modifying agents are indicated should be carefully considered. Our older patient had a progressive disease course, and neuroimaging studies did not reveal evidence of active disease. Based on this, a decision was made to monitor him clinically and radiologically. Management of spasticity with regular daily stretching exercises was discussed with him. A first clinical manifestation of multiple sclerosis can occur at a later-than-typical age. Most studies consider an onset at age 50 years or older to be late-onset multiple sclerosis, whereas first symptoms occurring at age 60 years or older are commonly referred to as very late–onset MS.

Behavioral Change, Seizures, and Temporal Lobe Lesion

A 56-year-old man with a history of type 2 diabetes, hypertension, hyperlipidemia, sleep apnea, alcohol use disorder in remission, renal cell carcinoma, and mucinous adenocarcinoma of the lung sought care for evaluation of presumed limbic encephalitis. Six months before evaluation, he had development of anxiety, fatigue, and blurry vision. He was diagnosed with renal cell carcinoma, which was resected. Subsequently, worsening depression developed, which required self-admitted psychiatric hospitalization for suicidal ideation. After discharge he had subacute development of aphasia, inability to recognize family members, and delusions for which he was hospitalized. Brain magnetic resonance imaging demonstrated a large, partly expansile, T2/fluid-attenuated inversion recovery–hyperintense lesion involving the left hippocampus and parahippocampal gyrus, as well as temporal neocortex and white matter, which was interpreted as limbic encephalitis. Spinal fluid analysis showed 66 total nucleated cells/μ‎L with 93% lymphocytes, normal cytologic findings, protein concentration of 66 mg/dL, and 15 erythrocytes/μ‎L. The Kokmen short test of mental status indicated mainly an amnestic profile without delirium, with a total score of 31 of 38. Given the patient’s neuroimaging findings for limbic encephalitis and lack of clear encephalopathy, the initial focus was confirming or ruling out the diagnosis of limbic encephalitis. He underwent repeated cerebrospinal fluid analysis, which showed 3 total nucleated cells/μ‎L with a protein concentration of 67 mg/dL. Serum autoantibody testing showed a low-titer glutamic acid decarboxylase 65-kDa isoform antibody value of 0.17 nmol/L. Brain magnetic resonance imaging 3 months after his initial magnetic resonance imaging showed slight progression of the expansile, left temporal lobe, T2-hyperintense lesion, further involving the left parietal lobe white matter, temporal lobe neocortex, and splenium of the corpus callosum, without clear gadolinium enhancement. A diagnosis of anaplastic astrocytoma (World Health Organization grade III) was made. He was treated with temozolomide and radiotherapy, with radiographic improvement. However, he had development of medically refractory focal seizures with secondary generalization. Approximately 3 years after his initial diagnosis, the patient experienced functional decline, with brain magnetic resonance imaging demonstrating multiple new, bihemispheric, T2-hyperintense lesions concerning for multifocal glioma. Given his poor prognosis and functional status, the patient was transitioned to comfort care. The presentation of disease in this patient highlights the importance of neuroimaging interpretation in the context of clinical history. Although this case patient had some features that could suggest a paraneoplastic limbic encephalitis—including behavioral changes, seizure, systemic malignancy, and apparent clinical response to immunosuppression—several features were inconsistent with this diagnosis.

Experimental Imaging Study of Encephalomalacia Fluid-Attenuated Inversion Recovery (FLAIR) Hyperintense Lesions in Posttraumatic Epilepsy

This study introduced new MRI techniques such as neurite orientation dispersion and density imaging (NODDI); NODDI applies a three-compartment tissue model to multishell DWI data that allows the examination of both the intra- and extracellular properties of white matter tissue. This, in turn, enables us to distinguish the two key aspects of axonal pathology—the packing density of axons in the white matter and the spatial organization of axons (orientation dispersion (OD)). NODDI is used to detect possible abnormalities of posttraumatic encephalomalacia fluid-attenuated inversion recovery (FLAIR) hyperintense lesions in neurite density and dispersion. Methods. 26 epilepsy patients associated with FLAIR hyperintensity around the trauma encephalomalacia region were in the epilepsy group. 18 posttraumatic patients with a FLAIR hyperintense encephalomalacia region were in the nonepilepsy group. Neurite density and dispersion affection in FLAIR hyperintense lesions around encephalomalacia were measured by NODDI using intracellular volume fraction (ICVF), and we compare these findings with conventional diffusion MRI parameters, namely, fractional anisotropy (FA) and apparent diffusion coefficient (ADC). Differences were compared between the epilepsy and nonepilepsy groups, as well as in the FLAIR hyperintense part and in the FLAIR hypointense part to try to find neurite density and dispersion differences in these parts. Results. ICVF of FLAIR hyperintense lesions in the epilepsy group was significantly higher than that in the nonepilepsy group ( P < 0.001 ). ICVF reveals more information of FLAIR(+) and FLAIR(-) parts of encephalomalacia than OD and FA and ADC. Conclusion. The FLAIR hyperintense part around encephalomalacia in the epilepsy group showed higher ICVF, indicating that this part may have more neurite density and dispersion and may be contributing to epilepsy. NODDI indicated high neurite density with the intensity of myelin in the FLAIR hyperintense lesion. Therefore, NODDI likely shows that neurite density may be a more sensitive marker of pathology than FA.

RARE PRESENTATION OF LHERMITTE-DUCLOS DISEASE

Lhermitte-Duclos disease (LDD) arises from an uncommon benign lesion which alters the normal cerebellar laminar pattern. This case report shows the imaging ndings of this condition in 39 year-old male, presented with history of headache and dizziness for duration of ten days. Intial assessment included a non-contrast CT which showed a mass in left cerebellar hemisphere with surrounding mass effect. MRI multiplanar sequences showed a well dened T2 hyperintense lesion with a tigroid appearance.The lesion showed a mild bright signal on diffusion-weighted images, whereas MR Spectroscopy shows reduced choline levels. Differential diagnosis in terms of imaging include subacute infarct, cerebellitis, glial tumor,encephalitis but these do not give the classical tigroid appearance on MRI. Lack of contrast enhancement , signicant diffusion and cellularity of the lesions can help in differentiating among them.