Peter R. Kinkel

Fatigue in multiple sclerosis and its relationship to depression and neurologic disability

We studied multiple sclerosis fatigue (MSF) and its relationship to depression and disability. Seventy-one patients [50 relapsing-remitting, 21 secondary progressive] were grouped by Fatigue Severity Scale (FSS) into MS-fatigue (MSF) (FSS55; n=46) or MS-nonfatigue (MSNF) (FSS44; n=20). Forty-one patients were grouped into MS-depression (MSD) (n=15) or MS-nondepression (MSND) (n=26) by interview. Higher expanded disability status scale (EDSS) scores were noted in MSF than MSNF patients (P=0.0003); EDSS scores correlated with FSS scores (rho=0.43, P=0.003). However, fatigue was present in 58% (n=29) of relapsing-remitting patients and in 52% (n=26) of patients with mild physical disability (EDSS53.5). Hamilton/Beck depression severity scores were higher in MSF than MSNF patients and correlated with FSS scores (P50.05). MSD had higher FSS scores than MSND patients (P=0.008). After controlling for EDSS, depression severity continued to correlate with FSS scores (rho=0.37, P=0.02). After controlling for depression, FSS scores no longer correlated with EDSS scores (rho=0.27, P=0.09). Thus, MSF is independent of physical disability, but is associated with depression, suggesting that common mechanisms play a role in MSF and MSD including psychological factors or brain lesions in specific neuroanatomic pathways. Further study is warranted to determine if antidepressant medications improve fatigue in MS.

Brain MRI lesions and atrophy are related to depression in multiple sclerosis

It is unclear whether brain MRI lesions are associated with depression in multiple sclerosis (MS). Neurological dysfunction in depressed (n = 19) and non-depressed (n = 29) MS patients was rated by expanded disability status scale (EDSS). EDSS was weakly predictive of the presence of (p = 0.03) and severity of (p = 0.01) depression. After correcting for EDSS, the presence of depression was predicted by superior frontal and superior parietal hypointense T1 lesions (p <0.01); the severity of depression was predicted by superior frontal, superior parietal and temporal T1 lesions, lateral and third ventricular enlargement, and frontal atrophy (p <0.01). Depression was not related to bright T2 lesions or enhancement. We conclude that atrophy and cortical–subcortical disconnection due to frontal and parietal white matter destructive lesions may contribute to depression in MS.

Fatigue in multiple sclerosis: Cross-sectional correlation with brain MRI findings in 71 patients

Article abstract Fatigue is an unexplained but common and disabling symptom in MS. We assessed fatigue in 71 patients with MS and identified MS–fatigue (MSF) and MS–nonfatigue (MSNF) groups. Fatigue severity did not correlate with regional or global MRI plaque load or atrophy assessed by conventional sequences. No significant differences were noted in any MRI measures between MSF and MSNF groups. We suggest that brain MRI disease topography or severity does not explain fatigue in MS and that fatigue is likely due to mechanisms poorly characterized by conventional MRI.

Thrombotic thrombocytopenic purpura: Brain CT and MRI findings in 12 patients

Article abstract Clinical-neuroimaging analysis of 12 thrombotic thrombocytopenic purpura (TTP) patients revealed a variety of brain lesions. These included reversible cerebral edema lesions with MRI features of reversible posterior leukoencephalopathy syndrome (RPLS). Most of the RPLS patients had hypertension and renal dysfunction, suggesting RPLS due to hypertensive encephalopathy. Prompt treatment usually led to neurologic recovery and disappearance of edematous lesions. Those with infarcts or hematomas had a poorer outcome. TTP should be added to the expanding spectrum of RPLS and hypertensive encephalopathy.

Occipital Lobe Seizures as the Major Clinical Manifestation of Reversible Posterior Leukoencephalopathy Syndrome: Magnetic Resonance Imaging Findings

Summary: Purpose: Reversible posterior leukoencephalopathy syndrome (RPLS) is an increasingly recognized brain disorder most commonly associated with malignant hypertension, toxemia of pregnancy, or the use of immunosuppressive agents. When associated with acute hypertension, RPLS typically occurs concurrently with the fulminant clinical syndrome of hypertensive encephalopathy. We describe occipital lobe seizures, in the setting of only moderate elevations of blood pressure, as the major clinical manifestation of RPLS.

MRI FINDINGS IN LUMBAR PUNCTURE HEADACHE SYNDROME: ABNORMAL DURAL-MENINGEAL AND DURAL VENOUS SINUS ENHANCEMENT

Intracranial hypotension (IH) is a treatable cause of persistent headaches. Persistent cerebrospinal fluid (CSF) leak at a lumbar puncture (LP) site may cause IH. We present postcontrast MRI of a patient with post-lumbar-puncture headache (LPHA) showing abnormal, intense, diffuse, symmetric, contiguous dural-meningeal (pachymeningeal) enhancement of the supratentorial and infratentorial intracranial dura, including convexities, interhemispheric fissure, tentorium, and falx. MRI also showed abnormal dural venous sinus enhancement, a new finding in LPHA, suggesting compensatory venous expansion. Thus, IH and venodilatation may play a role in the development of LPHA.

Magnetic resonance imaging findings in acute cerebellitis

Cerebellitis, also known as acute cerebellar ataxia, is an inflammatory syndrome of cerebellar dysfunction that may reflect an infectious, post-infectious, or post-vaccination disorder. We present serial magnetic resonance imaging (MRI) findings in a partially reversible, idiopathic cerebellitis. Bilateral cerebellar parenchymal abnormalities were noted, including hyperintensities on T2-weighted images and cerebellar swelling. After contrast administration, the cerebellum showed abnormal bilateral enhancement. The authors state this represents the first report of abnormal contrast enhancement in this condition. The MRI lesions most likely reflect the reversible, inflammatory nature of the syndrome.

Cranial magnetic resonance imaging findings in bacterial endocarditis: the neuroimaging spectrum of septic brain embolization demonstrated in twelve patients.

Infective endocarditis (IE) is an elusive systemic disorder that is often associated with neurologic complications. The contribution of brain magnetic resonance imaging (MRI) to the diagnosis of IE and the spectrum of such findings has been only sparsely described previously. The authors report cranial MRI findings in 12 patients with IE. Each of the patients had MRI evidence of cerebral embolization, with multiple brain lesions noted in most patients (n = 1 0). Cortical branch infarction was the most common lesion (n = 8), which usually involved the distal middle cerebral artery tree. The next most common finding (n = 7) was numerous small embolic lesions which typically lodged in the supratentorial gray‐white junction, some of which were clinically silent and many of which enhanced (probable microabscesses). Brain hemorrhages were noted in four patients, most commonly subarachnoid hemorrhage (n = 3). Two patients developed multiple frank parenchymal macroabscesses/cerebritis lesions. A previously unreported finding in septic embolization, a stroke that became infected with abscess formation (“septic infarction”), was noted in two patients. MRI showed orbital cellulitis in two patients. Most patients studied with gadolinium showed enhancement of lesions (n = 5/8). The authors conclude that cranial MRI may be a valuable tool in the evaluation of patients with IE. The presence of characteristic cranial MRI lesions, especially of multiple types, may prompt early diagnosis and treatment. Key words: MRI, brain, endocarditis, septic emboli, abscess, stroke, orbital infection.

Cognitive impairment after acute supratentorial stroke : a 6-month follow-up clinical and computed tomographic study

SummaryTo document the occurrence, time course, and predictors of global cognitive impairment following a supratentorial stroke, we prospectively studied 41 consecutive patients with acute cerebral ischemia and no evidence of pre-existing intellectual disturbances. The Graded Neurologic Scale and Mattis Dementia Rating Scale were used to assess neurologic and cognitive deficits within the first week, 3 weeks and 6 months after the onset of symptoms. CT was performed at each examination and semiquantitative measurements of infarct volumes and brain atrophy were obtained. Sixty-one percent of patients were found to be cognitively impaired within the first week. After 6 months this deficit had resolved in 24%, but was still present in 37% of individuals. Initial findings associated with a high risk of longterm intellectual dysfunction were: 1. moderately severe cognitive impairment, 2. diminished alertness in the acute stroke stage, 3. infarction involving the temporal lobe, 4. evidence of multiple brain infarcts and 5. pronounced ventricular enlargement. Logistic regression analysis revealed temporal infarcts and evidence of multiple ischemic lesions as the most powerful predictors of persistent cognitive impairment. By these two factors alone, 85.4% of study participants could be correctly classified regarding their cognitive outcome. These results suggest cognitive dysfunction to be a frequent sequela of supratentorial stroke. Its long-term persistence may be predicted on the basis of certain features.

CEREBRAL VENOUS INFARCTIONS PRESENTING AS ENHANCING SPACE-OCCUPYING LESIONS : MRI FINDINGS

Cerebral venous thrombosis is an unusual form of cerebrovascular disease that may cause cerebral venous infarction (CVI). Magnetic resonance imaging (MRI) of the brain may improve the often elusive diagnosis of CVI. However, the sensitivity, specificity, and full spectrum of such MRI findings are poorly understood. The authors present the cases of three patients with CVI whose MRI scans showed abnormally enhancing tumor‐like brain lesions. Two of the CVIs were hemorrhagic and exerted mass effect. One patient showed increasingly nodular and heterogeneous ring‐like enhancement progressing from the single‐dose to the triple‐dose gadolinium contrast images. The CVI of a second patient also showed ring‐like enhancement. Biopsy was performed on one of these patients and was strongly considered for the other two patients to exclude neoplastic disease. Careful examination of the MRI appearance of venous structures and the use of specialized MRI techniques improved the recognition of CVI for two patients and prevented biopsy. This represents the first description of abnormal tripledose MRI contrast enhancement in CVI. Consideration of CVI in the care of patients with enhancing tumor‐like masses may lead to earlier diagnosis and treatment, preventing unnecessary invasive diagnostic procedures. CVI should be added to the differential diagnosis of supratentorial ring‐enhancing masses.