Cognitive Impairment in Patients With Clinically Isolated Lesions of the Type Seen in Multiple Sclerosis

Callanan, Margie; Logsdail, Stephen; Ron, María A.; Warrington, Elizabeth K.

doi:10.1093/brain/112.2.361

Cited by 115 publications

(47 citation statements)

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“…They found that severe fatigue in MS is associated with a reduction in glucose metabolism in the prefrontal cortex, adjacent white matter and basal ganglia, and concluded that fatigue may result from demyelination of the frontal white matter. This is consistent with the previously reported correlation between fatigue and impaired cognition in the early stages of MS. 21 The possibility that fatigue may indicate primary demyelination or axonal damage in the cerebrum has implications for the treatment of MS. If this is confirmed by further research, severe fatigue may itself become an indication for the treatment of MS in order to minimize further CNS damage.…”

Section: Mechanism Of Fatiguementioning

confidence: 99%

Recent progress in the diagnosis and treatment of multiple sclerosis

Pender

1999

Journal of Clinical Neuroscience

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Magnetic resonance imaging (MRI) now provides valuable diagnostic and prognostic information for the management of multiple sclerosis (MS) but the diagnosis still largely rests on the clinical features of central nervous system (CNS) lesions disseminated in time and place. Recent histological and MRI studies indicate that extensive axonal damage can occur in MS, even early in the disease course, and is likely to be an important cause of accumulating disability. Several immunomodulating agents have now been shown to have beneficial effects in MS. High dose intravenous or high dose oral methylprednisolone therapy accelerates recovery from attacks of relapsing-remitting MS, but at present there is no convincing evidence that standard dose (intermediate dose) oral corticosteroid therapy is beneficial for such attacks. Interferon beta, copolymer 1 (glatiramer acetate) and i.v. immunoglobulin therapy each significantly reduce the frequency of attacks of relapsing-remitting MS. Interferon beta also inhibits the progression of disability in relapsing-remitting MS and secondary progressive MS, but its effect on primary progressive MS is unknown. Oral low dose methotrexate therapy slows the progression of disability in secondary progressive MS and possibly in primary progressive MS, but it is likely that the currently used dosage (7.5 mg weekly) is suboptimal. Further research is needed to determine the optimal doses and combinations of the above therapies in MS and to develop better therapies, particularly for primary progressive MS.

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Section: Mechanism Of Fatiguementioning

confidence: 99%

Recent progress in the diagnosis and treatment of multiple sclerosis

Pender

1999

Journal of Clinical Neuroscience

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“…33 Slowed cognitive processing is present early in the disease and can be seen in people with clinically isolated syndromes -a single episode of demyelination in one area of the CNS, eg optic neuritis or brainstem or spinal cord syndrome -with asymptomatic lesions elsewhere in the brain on MRI. 34 In people with established MS, around 40 per cent have cognitive abnormalities. 35 Risk factors for impaired cognitive function in MS are age greater than 40 years, low premorbid intelligence or educational attainment, and depression.…”

Section: Cognitive Disordersmentioning

confidence: 99%

Management of neuropsychiatric symptoms in multiple sclerosis

Sommerlad¹,

Price²,

Trip³

2014

Prog Neurol Psychiatry

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M ultiple sclerosis (MS) is the commonest cause of neurological disability in young and middleaged adults. 1 The characteristic pathological features are demyelinating plaques, astrocytic gliosis and immune-mediated inflammation anywhere within the CNS, with the periventricular region, brainstem, juxta cortical region, optic nerves and spinal cord being particularly common targets. The neurological manifestations are diverse, although they usually reflect the function of the affected anatomical site, and the course of the illness is variable and initially difficult to predict with accuracy.In 80-90 per cent of cases, MS is relapsing-remitting in nature with two-thirds of these cases developing a secondary progressive form of the condition a variable number of years after onset and a third having a relapsing-remitting course that does not result in long-term serious disability. The remaining 10-20 per cent of patients have a primary progressive course with gradually worsening symptoms. 2 The prognosis can be poor in the long term but progression is frequently slow; recent evidence suggests a median of 28 years before a stick is required for walking. 3 The UK annual incidence of MS is 10 in 100 000 with a prevalence of 200 in 100 000. 4 There is estimated to be over 100 000 people suffering from the condition in the UK. The median age of onset is 31 years and it is approximately twice as common in women. 5 It has a multifactorial aetiology with genetic and environmental factors shown to be important. There is 31 per cent monozygotic concordance compared to 5 per cent in dizygotic twins 6 while the environmental influence is demonstrated by marked variations in prevalence in genetically homogenous populations. 7 Prevalence increases with increasing distance from the equator and those who emigrate in childhood have prevalence rates consistent with their adopted country. 8 MS commonly presents with weakness, tingling or numbness in the limbs; diplopia, visual loss or impaired visual acuity; vertigo; dysarthria and ataxia; fatigue; and bladder and bowel disturbance. 5 The array of presenting symptoms in MS can lead to diagnostic uncertainty and neuropsychiatric conditions such as somatisation disorder are sometimes suspected. A study demonstrated that 16 per cent of patients with MS had been referred to a psychiatrist between the onset of neurological symptoms and diagnosis of MS. In spite of neurological symptoms being present in the majority of cases, these remained largely overlooked and diagnoses of conversion disorder and hysterical personality disorder were applied, 9 although the increased use of MRI scans since this finding was reported has improved diagnostic accuracy. While neurological features are the most recognised manifestations of MS, psychopathology, including affective, psychotic and cognitive disorders, is also common. The identification of these symptoms is often more difficult and diagnosis can be delayed. Psychiatric symptoms can occur at onset or later in the MS disease process and initial psych...

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“…Nevertheless, the effect of cognitive impairment on everyday life activities, employment status, and social relationships is considerable (Amato et al, 1995;Rao et al, 1991b). Cognitive impairment may occur in the earliest stages of the disease (Achiron & Barak, 2003;Callanan et al, 1989;Deloire et al, 2005;Feinstein et al, 1992;Glanz et al, 2007) even in patients with clinically isolated syndrome (CIS) (Achiron & Barak, 2003;Feuillet et al, 2007;Glanz et al, 2007;Potagas et al, 2008). Cognitive deficits may develop independently from physical disability particularly in the early stage of the disease and in patients with benign MS (Feuillet et al, 2007;Glanz et al, 2007;Portaccio et al, 2009).…”

Section: Introductionmentioning

confidence: 99%