Peter O Jenkins

Concussion is confusing us all

It is time to stop using the term concussion as it has no clear definition and no pathological meaning. This confusion is increasingly problematic as the management of ‘concussed’ individuals is a pressing concern. Historically, it has been used to describe patients briefly disabled following a head injury, with the assumption that this was due to a transient disorder of brain function without long-term sequelae. However, the symptoms of concussion are highly variable in duration, and can persist for many years with no reliable early predictors of outcome. Using vague terminology for post-traumatic problems leads to misconceptions and biases in the diagnostic process, producing uninterpretable science, poor clinical guidelines and confused policy. We propose that the term concussion should be avoided. Instead neurologists and other healthcare professionals should classify the severity of traumatic brain injury and then attempt to precisely diagnose the underlying cause of post-traumatic symptoms.

Catecholamines and cognition after traumatic brain injury

Cognitive impairment following traumatic brain injury is common, poorly understood and difficult to treat. Jenkins et al. review evidence that disruption to certain neurotransmitters (dopamine and noradrenaline) is a common cause of these persistent cognitive impairments and propose using neuroimaging techniques to guide treatment selection and monitor response.

Prevalence and correlates of vitamin D deficiency in adults after traumatic brain injury

Traumatic brain injury (TBI) is a major cause of long‐term disability with variable recovery. Preclinical studies suggest that vitamin D status influences the recovery after TBI. However, there is no published clinical data on links between vitamin D status and TBI outcomes. The aim was to determine the (i) prevalence of vitamin D deficiency/insufficiency, and associations of vitamin D status with (ii) demographic factors and TBI severity, and with (iii) cognitive function, symptoms and quality of life, in adults after TBI.

Minocycline reduces chronic microglial activation after brain trauma but increases neurodegeneration

Head injury survivors can develop neurodegeneration associated with persistent neuroinflammation, but whether the latter is harmful or beneficial is unclear. Scott et al. report that minocycline reduces neuroinflammation months and years after injury but increases a blood marker of neurodegeneration, suggesting that persistent neuroinflammation has reparative effects long after injury.

Serum insulin-like growth factor-I levels are associated with improved white matter recovery after traumatic brain injury

Traumatic brain injury (TBI) is a common disabling condition with limited treatment options. Diffusion tensor imaging measures recovery of axonal injury in white matter (WM) tracts after TBI. Growth hormone deficiency (GHD) after TBI may impair axonal and neuropsychological recovery, and serum insulin‐like growth factor‐I (IGF‐I) may mediate this effect. We conducted a longitudinal study to determine the effects of baseline serum IGF‐I concentrations on WM tract and neuropsychological recovery after TBI.

Serum IGF-I levels are associated with improved white matter recovery after TBI

Traumatic brain injury (TBI) is a common disabling condition with limited treatment options. Diffusion tensor imaging measures recovery of axonal injury in white matter (WM) tracts after TBI. Growth hormone deficiency (GHD) after TBI may impair axonal and neuropsychological recovery, and serum insulin‐like growth factor‐I (IGF‐I) may mediate this effect. We conducted a longitudinal study to determine the effects of baseline serum IGF‐I concentrations on WM tract and neuropsychological recovery after TBI.

Altered caudate connectivity is associated with executive dysfunction after traumatic brain injury

Traumatic brain injury often produces executive dysfunction, causing long-term problems with behaviour and personality. De Simoni et al. report that executive dysfunction following TBI is associated with altered corticostriatal interactions important for behavioural control. These findings provide a target for the evaluation of treatments aimed at improving executive function after TBI.

Multiple sclerosis presenting as a relapsing amnestic syndrome

Although neuropsychiatric symptoms are increasingly recognised in early established multiple sclerosis,1–3 it is unusual for patients to present with solitary cognitive or neuropsychiatric symptoms,4–12 including depressive symptoms4–7 ,10 ,11 and progressive cognitive decline.6 ,8 ,9 ,11 ,12 Here, we present a case of multiple sclerosis that presented as a relapsing amnestic syndrome with only very mild underlying cognitive changes. A previously fit 76-year-old man reported a 2–3-h episode of agitation and confusion. During this, he became repetitive and obsessive and had no memory of this period afterwards. Following the event, his wife noticed that his memory was not quite as good as previously (particularly for peoples names), but otherwise he had no residual cognitive or physical deficits. His wife also reported that the year before …

Systemic Lupus Erythematosus Presenting as Orbital Myositis

Abstract The authors present a case of diplopia and eye pain due to orbital myositis in a patient with a de novo diagnosis of systemic lupus erythematosus. Systemic lupus erythematosus is a rare cause of orbital myositis and should be considered when other, more common, conditions have been excluded.

Dopaminergic abnormalities following traumatic brain injury

Traumatic brain injury can reduce striatal dopamine levels. The cause of this is uncertain, but is likely to be related to damage to the nigrostriatal system. We investigated the pattern of striatal dopamine abnormalities using 123I-Ioflupane single-photon emission computed tomography (SPECT) scans and their relationship to nigrostriatal damage and clinical features. We studied 42 moderate-severe traumatic brain injury patients with cognitive impairments but no motor parkinsonism signs and 20 healthy controls. 123I-Ioflupane scanning was used to assess dopamine transporter levels. Clinical scan reports were compared to quantitative dopamine transporter results. Advanced MRI methods were used to assess the nigrostriatal system, including the area through which the nigrostriatal projections pass as defined from high-resolution Human Connectome data. Detailed clinical and neuropsychological assessments were performed. Around 20% of our moderate-severe patients had clear evidence of reduced specific binding ratios for the dopamine transporter in the striatum measured using 123I-Ioflupane SPECT. The caudate was affected more consistently than other striatal regions. Dopamine transporter abnormalities were associated with reduced substantia nigra volume. In addition, diffusion MRI provided evidence of damage to the regions through which the nigrostriatal tract passes, particularly the area traversed by dopaminergic projections to the caudate. Only a small percentage of patients had evidence of macroscopic lesions in the striatum and there was no relationship between presence of lesions and dopamine transporter specific binding ratio abnormalities. There was also no relationship between reduced volume in the striatal subregions and reduced dopamine transporter specific binding ratios. Patients with low caudate dopamine transporter specific binding ratios show impaired processing speed and executive dysfunction compared to patients with normal levels. Taken together, our results suggest that the dopaminergic system is affected by a moderate-severe traumatic brain injury in a significant proportion of patients, even in the absence of clinical motor parkinsonism. Reduced dopamine transporter levels are most commonly seen in the caudate and this is likely to reflect the pattern of nigrostriatal tract damage produced by axonal injury and associated midbrain damage.