ischaemic stroke [4, 5]. A review of important opportunistic infections (specically tuberculous and cryptococcal meningitis) common in HIV, their cerebrovascular complications and the role of neurosonology in their diagnosis and monitor­ing is presented below.

ONSD measured by ultrasound is able to determine the presence of intracranial hyperten­sion with reasonable accuracy in TBM [16]. However, its potential role in the management of TBM has yet to be established. Ultrasound ONSD could be of great utility in the diagnosis of neurological deterioration in TBM—a raised ONSD in a patient deteriorating neurologically could signify the development of hydrocephalus which would warrant an urgent CT scan and pos­sibly neurosurgical intervention, whereas a nor­mal ONSD in the same patient may indicate other complications of TBM such as hyponatraemia, seizures or stroke.

Transcranial Doppler ultrasound has been used for the diagnosis and monitoring of TBM

vasculopathy. To our knowledge, ve authors have published their experience of using TCD to diagnose and monitor TBM-related vasculopa­thy (Table 20.1) [26–30]. Kilic et al. identied three phases of TBM vasculopathy based on clinical and sonographic ndings (Table 20.2) [30]. Interestingly, the authors likened the nd- ings on TCD examination in phase 1 to those seen in the early stages of acute vasospasm fol-

label, randomised controlled trial demonstrated that ‘triple H’ therapy (hypervolaemia­hypertension- haemodilution—used extensively in vasospasm in SAH) is safe and feasible in TBM and a trend towards improvement in focal neurological decits and mentation was found [28]—however, the conclusions that can be drawn from this study are limited given its small sample size (n=12).

lowing aneurysmal subarachnoid haemorrhage (SAH) [30]. If vasospasm is involved in the pathophysiology of stroke in TBM and TCD is

world [53]. Evidence from autopsy studies sug­gests that adhesion of parasitised erythrocytes (PEs) to the microvascular endothelium leading to their sequestration in microvessels is the path­ological hallmark of adult and paediatric CM [54, 55]. CM can be dened clinically as coma in the presence of a peripheral Plasmodium falci- parum parasitaemia in the absence of another identiable cause of coma [56]. However, approximately one-quarter of patients meeting this clinical denition do not have evidence of sequestration of parasitised RBCs at autopsy [55]. Impaired consciousness in the context of severe malaria may be due to other causes such as a prolonged postictal state following febrile seizure or metabolic derangements such as aci­dosis or hypoglycaemia [57]. More recently, the presence of malarial retinopathy has been sug­gested as an important diagnostic sign for paedi­atric CM [58]. Malarial retinopathy accurately predicts the degree of sequestration of parasit­ised red blood cells (PRBCs) in the cerebral microvasculature [55, 59], presence of brain haemorrhages [60] and prognosis [61]. As such, it has been proposed that retinopathy-positive (RN-positive) paediatric CM is a distinct entity in which neurovascular disturbance is a charac­teristic component of the pathophysiology of the disease. Mortality from retinopathy-positive (RN-positive) paediatric CM remains high at approximately 14% [62] despite appropriate treatment with artesunate. Moreover, approxi­mately one-third of survivors of RN-positive paediatric CM will develop long- term neurologi­cal sequelae, including epilepsy, motor, sensory or language decits [63]. Despite this, the patho­physiology of paediatric CM remains poorly understood and few adjunctive therapies to anti­malarials have been developed that are success­ful in improving the outcome [64].

come in paediatric CM [65]. Intracranial hyperten­sion (ICH) has been demonstrated in African children by raised cerebrospinal uid (CSF) open­ing pressure on lumbar puncture (LP) [66–68] and intraparenchymal intracranial pressure (ICP) mon­itoring [65]. The pathophysiology of ICH in paedi­atric CM remains unclear. Increased brain volume has previously been demonstrated in African chil­dren using CT (dened as loss of CSF spaces) [69] and MRI [70]. Various mechanisms have been pro­posed for this increased brain volume, including vasogenic oedema due to blood-brain barrier (BBB) breakdown [71, 72], cytotoxic oedema from impaired perfusion leading to cell death [73], sequestration of PRBCs in postcapillary venules leading to obstruction and vascular congestion [54], diffuse cerebral microhaemorrhages [72] and hyperaemia due to seizures, anaemia and/or fever leading to autoregulatory dysfunction.

impaired consciousness) underwent TCD exami­nation [77]. Based on ndings on TCD examina-

However, the publication of the ndings from BEST:TRIP and their interpretation prompted considerable debate in the literature and some have interpreted the trial as indicating that ICP monitoring has no role in low-resource settings. As such, a consensus-based interpretation was subsequently published by the authors [99]. Of note, one of the statements included was that the ndings from the trial should be ‘applied cau­tiously to regions with much different treatment milieu’. In consideration of this, it should be noted that there is considerable variability in the resources available for neurotrauma care between and even within LMICs. For example, many hos­pitals in sub-Saharan Africa and Asia do not have the capacity to perform serial CT scans on severe TBI patients or regularly administer neuroprotec­tive treatments (such as mannitol, hypertonic saline or barbiturates) to them as was done in in the ICE arm of the study. Moreover, there is emerging evidence to suggest that ICP monitor­ing does add benet in certain, specic settings in LMICs. A single-centre retrospective cohort study from Kerala in India found that ICP moni­toring of severe TBI patients with diffuse brain injury was associated with a decreased need for neuroprotective management, radiation exposure and length of ICU stay [99]. In addition, improved functional outcome was observed at 1 month (although this was not observed at 3 and 6months). As such, given the barriers to deploy­ing ICP monitoring in many institutions in LMICs, an inexpensive, accurate method of esti­mating ICP may be of benet in guiding treat­ment decisions in TBI in this population. To our knowledge, no studies have been published examining the utility of neurosonology in man­aging moderate and severe TBI in low-resource settings where ICP monitoring is unavailable but, at the time of publication, research projects are ongoing in Ethiopia and Zambia. This research area is one of the most promising potential appli­cations of neurosonology in tropical medicine, especially as a means of augmenting existing clinical practise guidelines for moderate and severe TBI in LMICs which rely on imaging and clinical examination alone.