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First published online March 28, 2007
British Journal of Radiology (2007) 80, 422-429
© 2007 British Institute of Radiology
doi: 10.1259/bjr/81758556
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Spectrum of radiological changes in hypertensive children with reversible posterior leucoencephalopathy

N Prasad, MD, DNB, DM, DNB, MNAMS 1 S Gulati, DM 1 R K Gupta, MD 2 K Sharma, MD 3 K Gulati, MD 2 R K Sharma, FASN 1 and A Gupta, DNB 1

Departments of 1 Nephrology, 2 Radiology and 3 Neuro-opthalmology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India

Correspondence: Dr Sanjeev Gulati, Department of Nephrology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Raebareli Road, Lucknow 226014, India. E-mail: sgulati{at}sgpgi.ac.in


   Abstract
Top
 Abstract
Introduction
 Methods and materials
 Results
 Discussion
 References
 
We prospectively studied 19 children with severe hypertension to evaluate the spectrum of radiological changes, severity and reversibility of this entity. All of them were subjected to clinical and biochemical evaluation, followed by magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA). Headache was seen in 17 children, 13 had confusion and drowsiness, 12 had nausea and vomiting, 10 patients had visual disturbances, seizure and dyspnoea. Only two had focal neurological deficit (one with right facial palsy and another with right lateral rectus palsy). Of these 19 children, 15 patients had hypertensive retinopathy and four had normal fundi. The positive MRI findings in 17/19 patients were: bilateral leukoencephalopathic changes in occipitoparietal region (9/17), diffuse white/grey matter lesion (3/17) patients, brain stem hyperintensity (2/17) and haemorrhagic lesions (3/17). On MRA, 12/19 patients had attenuation of cerebral arteries of different degree. On follow up, MRI findings resolved in all except three patients. All patients had normal MRA on follow up, except one with persistent minimal attenuation of middle cerebral artery and another had spasm in anterior, middle and posterior cerebral arteries. The intracranial abnormalities in these patients with severe hypertension were reversible in many of the cases after control of blood pressure was achieved. We therefore conclude that severe hypertension may lead to leuoencephalopathy, which had a wide radiological spectrum. A better understanding of this complex syndrome may obviate unnecessary investigations and allow management of associated problems in prompt and appropriate ways.


   Introduction
Top
 Abstract
 Introduction
Methods and materials
 Results
 Discussion
 References
 
Reversible posterior leuoencephalopathy syndrome (RPLS) is characterized clinically by severe hypertension and radiological involvement of the white matter in the posterior portion of the cerebral hemispheres [1]. Rarely, involvement of brain stem, cerebellum, basal ganglia, frontal and parietal lobes has also been reported [1–3]. There have been several case reports of reversible leuoencephalopathy consequent upon malignant hypertension associated with post-streptococcal glomerulonephritis [4], minimal change disease [5], hepatitis C virus-positive patients on long-term haemodialysis [6], ciclosporin and tacrolimus therapy [7] and eclampsia [3, 8].

The majority of patients with RPLS are adults [9]. Its true prevalence may be underestimated in children [10, 11]. Recently there have been reports of RPLS in children consequent upon chemotherapy in patients with leukaemia and lymphoma [11–13] and tumour lysis syndrome [14]. Jones et al [10] reported neuroimaging of brain in five cases of hypertension in children.

Acute rise in blood pressure is usually the cause of this syndrome. Uraemic encephalopathy represents additional aetiologies of RPLS which have a greater tendency for central distribution for unknown reasons [15]. However the tendency for central distribution in uraemic patients remains to be confirmed.

Hence we prospectively studied 19 children with severe hypertension for posterior leuoencephalopathy to characterize the spectrum of radiological changes and reversibility on MRI. This is to date the largest study on reversible posterior leuoencephalopathy syndrome in the paediatric age group.


   Methods and materials
Top
 Abstract
 Introduction
 Methods and materials
Results
 Discussion
 References
 
We prospectively studied 19 children with severe hypertension (greater than 99th percentile for age) referred to the emergency department of our institute. All patients were evaluated at presentation clinically for headache, nausea, vomiting, visual symptoms, seizure, focal neurological deficit, dyspnoea and degree of hypertension. A detailed clinical examination (including neurological and fundus) was carried out in every patient. Severe hypertension was defined as blood pressure above the 99th percentile for age and height as per the Revised Task Force criteria [16] with or without clinical evidence of seizure, focal deficit and Grade 3 or 4 retinopathy. The exclusion criteria were as follows: (1) patients above 16 years of age, (2) patients on immunosuppressive therapy, and (3) mild and moderate hypertension (as per the Revised Task Force criteria). All patients were subjected to detailed haematological and biochemical tests, ultrasonography of abdomen, kidney, ureter and bladder region, captopril renogram with 99Tcm - diethylenetriaminepentaacetic acid (DTPA) [17]. The diagnosis of aortoarteritis was made by the presence of classical arteriographic changes, i.e. multifocal areas of stenosis, irregularity or aneurysmal dilatation of the aorta or its major branches. This was confirmed by digital subtraction angiography of the aorta and renal vessels [18]. Digital subtraction angiography was done on an Advantx LCA plus (GE Medical Systems, USA) machine in patients with clinical diagnosis of renovascular hypertension. A diagnosis of aortoarteritis was made based on criteria such as the presence of symptoms and signs of ischaemic, inflammatory large vessel disease in the form of constitutional symptoms, claudication, abdominal or peripheral bruit, asymmetry of pulses, hypertension and classical arteriographic changes, i.e. multifocal areas of stenosis, irregularitity and aneurysmal dilatation of the aorta or its major branches [18].Go


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  		Table 1. Demographic profile and characteristics of patients

 
At the time of presentation, MRI studies were performed on a 1.5 T superconducting system with a circularly polarized head coil. The brain MRI protocol included axial spin-echo. T1 weighted (repetition time (TR)/echo time (TE)/excitations (n) = 550/14/3) and T2 weighted (TR/TE/n = 2200/20, 80/1) images were obtained with a 192 x 256 matrix, 5 mm thick sections and a 0.5 mm intersection space. Magnetic resonance angiograms (MRAs) were obtained with a three-dimensional time of flight magnetization transfer prepared sequence. Gradient recalled echo (GRE) with or without phase imaging was also performed. MRI and MRA were done in all patients at presentation. The blood pressure was controlled using appropriate anti-hypertensive medications. Repeat MRI and MRA studies using the same protocol were done 4–8 weeks after the control of blood pressure with the same imaging criteria in all patients.


   Results
Top
 Abstract
 Introduction
 Methods and materials
 Results
Discussion
 References
 
There were 19 children with mean age 12±4 years (range 4–16 years). All of them had severe hypertension as per the Revised Task Force criteria. Of these, there were 13 boys and six girls. The mean systolic blood pressure (SBP) was 178±56 mmHg (range 160–240 mmHg) and diastolic blood pressure (DBP) was 118±37 mmHg (range 100–146 mmHg). Nine patients had aortoarteritis, five had diffuse proliferative glomerulonephritis, two haemolytic uraemic syndromes (HUS), one had reflux nephropathy, one lupus nephritis and one had renal limited crescentic glomerulonephritis (Table 1Go). All patients with diffuse proliferative glomerulonephritis had post-streptococcal glomerulonephritis. On clinical evaluation headache was the commonest symptom (17/19), followed by drowsiness and confusion (13/19), nausea and vomiting (12/19), visual disturbances (10/19), seizure (10/19) and dyspnoea (10/19), focal neurological deficit (2/19), while one child had a right rectus muscle palsy and another child had a right facial palsy. Four patients had normal fundus, while the rest had hypertensive retinopathy. Of these, six patients had papilloedema, six had retinal haemorrhage, two had A-V nipping with retinal haemorrhage and one had copper wire appearance and retinal haemorrhage. The number of medications required for control of hypertension was two to five anti-hypertensive drugs. The drugs used for control of hypertension included calcium channel blockers (nifedipine and amlodepin), beta- and alpha-blockers, angiotensin converting enzyme (ACE) inhibitors, angiotensin 2 receptor blockers, diuretics and clonidine. None of these patients was on immunosuppressive medications or steroids (including the patient with lupus nephritis) at the time of the initial MRI scan. The mean SBP and DBP were 132 mmHg (range 110–140) and 78 mmHg (range 70–90), respectively, at follow up. In our study there was no correlation of the outcome with the age, aetiology or severity of hypertension and time to achieve control of blood pressure. Twelve out of 19 patients had renal failure (serum creatinine >1.4 mg dl–1). Of these 12 patients, 11 had leukoencephalopathic changes and only one had initial normal MRI scan. Of these 12 patients, eight had attenuation of different degrees of vessels on initial MRA. Six out of seven patients with normal renal function had abnormal intracranial MRI findings on the initial MRI. Out of these six patients, three had persisting residual lesion on follow up MRI scan. The lesions appeared hyperintense on T1 and hypo- to isointense on T2 imaging. Of seven patients with normal renal function, five had abnormal MRA on presentation.

MRI scan has revealed leuoencephalopathy changes in 17/19 patients while it was normal in 2/19 patients. Of these 9/17 had leukoencephalopathic changes in the occipitoparietal region, bilaterally. Of these, four patients had only these lesions, three had additional involvement of in the frontal region (GoFigures 1 and 2Go) and two in the temporal region. The diffuse white and grey matter lesion was seen in three patients. Of these one had a diffuse white matter hyperintense lesion in the occipito-parietal, temporal and frontal region and the other two had hyper-intensity in the cerebral cortex, the subcortical white matter and the occipital, frontal and temporal regions. On T2 weighted image, hyperintensity of the pontine region of the brain stem was seen in two patients. Three patients had haemorrhagic lesions; of these, one patient had a haemorrhage in the left temporal region (Figure 3Go) and right frontal cistern, another had multiple haemorrhages in the temporal and frontal regions bilaterally and a third one had haemorrhage in the left basal ganglia region. Of these three patients with haemorrhagic lesions, two had additional white matter changes in the occipitoparietal region and one had a diffuse white matter lesion consistent with leukoencephalopathic changes. Two patients had normal MRI findings despite severe hypertension. It is possible that autoregulatory spasm may have prevented hyperperfusion injury and development of leukoencephalopathic changes in them. CT scanning was not done in any of the cases. In the present study, fluid-attenuated inversion-recovery (FLAIR) and diffusion-weighted imaging (DWI) were not done. However these have been shown to be useful in predicting non-reversibility in RPLS [19].


Figure 1
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  		Figure 1. A child with reversible leukoencephalopathy.T2 weighted axial images through the supraventricular regions (a) shows multiple hyperintensities in both occipital and frontal regions involving the cortex and subcortical white matter. Repeat T2 weighted axial image corresponding to (b) after 12 weeks shows normal imaging.

 

Figure 2
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  		Figure 2. Residual changes in a child with hypertensive leukoencephalopathy.T2 weighted axial images through the lateral ventricles (a) shows multiple hyperintensities in both occipital and frontal regions involving the cortex and subcortical white matter. Three-dimensional time of flight (3D-TOF) MR angiogram (b) shows only spasm of both proximal middle cerebral arteries (arrows). Repeat T2 weighted axial image (c) corresponding to (a) after 12 weeks shows residual lesions in both frontal regions.

 

Figure 3
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  		Figure 3. Leukoencephalopathy with left temporal bleed.T2 weighted axial image through the temporal lobe (a) shows hypointense lesion in the left temporal lobe (arrow) that shows a bloom effect on T2* weighted image (b) consistent with bleed.

 
On MRA, 12/19 patients had attenuation of the cerebral arteries; in seven patients the MRA was normal. All vessels, middle cerebral artery (MCA), anterior cerebral artery (ACA) and posterior cerebral artery (PCA) were attenuated in five patients, only posterior in three patients, only MCA in two patients; one had attenuation of middle and anterior and another one had middle and posterior. Of the two patients with only MCA attenuation, one had isolated left-sided attenuation while the other had peripheral filling defects as well. There was only one patient who had attenuation on MRA with a normal spin echo image on MRI on follow up scan (Figure 4Go). The attenuation in vessels was present in the very proximal region. All patients were asymptomatic after a mean follow up of 4 weeks of control of hypertension. The focal neurological deficit had improved completely in the patient with 6th cranial nerve palsy and partially in 7th nerve palsy.


Figure 4
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  		Figure 4. Normal imaging in a child with acute hypertensive encephalopathy.T2 weighted axial image (a) through the ventricles shows no abnormality. Three-dimensional time of flight (3D-TOF) MR angiogram (b) shows spasm of the left proximal and distal middle cerebral arteries (arrows).

 
On follow up, MRI scan was normal in 16 patients, while three patients had persistent abnormalities. Of these, one had residual haemorrhage in left basal ganglia, another had bilateral multiple white matter abnormalities in the frontal lobes (Figure 2Go) while a third had resolving residual haemorrhage. Thus leukoencephalopathic changes were reversible in all (Figure 1bGo) except three children: of these aortoarteritis was the cause of hypertension in two patients and another one had lupus nephritis. Of the two patients with aortoarteritis, one had a haemorrhagic lesion and another had a diffuse white matter lesion. The patient with lupus nephritis also had a haemorrhagic lesion.

On follow up 10 out of 12 now had normal MRA, while two patients had persistent abnormalities: one with persisting minimal attenuation of vessels and another who had spasm in all vessels. Of these one patient had lupus nephritis and another had haemolytic uraemic syndrome.


   Discussion
Top
 Abstract
 Introduction
 Methods and materials
 Results
 Discussion
References
 
This is the largest study to show the wide spectrum of involvement of brain lesions in reversible leuoencephalopathy, particularly in children. In this study, we prospectively observed RPLS in 17/19 children with severe hypertension (mean SBP 178mmHg and DBP 118 mmHg). Out of 17 children with various lesions, 14 had complete resolution of lesions on control of hypertension (mean SBP 132 mmHg and DBP 78 mmHg) and three had shown a trend towards resolution of the lesion. In recent years, this syndrome has been known by several names including hypertensive encephalopathy, hyperperfusion encephalopathy, reversible encephalopathy, occipitoparietal encephalopathy and reversible posterior cerebral oedema syndrome [15].

In our patients, headache was the commonest symptom followed by nausea and vomiting, drowsiness and confusion, visual disturbances, seizure, dyspnoea and focal neurological deficit. An almost similar clinical spectrum has been reported in the literature [1]. All patients were asymptomatic on follow up.

In this study, we have shown the wide spectrum of leukoencephalopathic changes varying from the most common involvement of the posterior portion of the cerebral hemisphere occipitoparietal lesion to less commonly reported lesions like involvement of the brain stem, cerebellum, basal ganglia, frontal and temporal lobes. RPLS is commonly seen in the occipitoparietal region but involvement of additional areas of the brain such as brain stem, cerebellum, basal ganglia, frontal and temporal lobes has also been reported in different studies [1–3]. Casey and Truwtt [15] have also discussed the wider spectrum of imaging appearances of this condition. Uraemic encephalopathy represents an additional aetiology of RPLS which has a greater tendency to central distribution for unknown reasons [15]. In our series, only two patients had brain stem lesions and one had a basal ganglia lesion. We have not found any predilection for central distribution of leukoencephalopathic changes in patients with renal failure in our series.

The common causes of hypertension in children are renoparenchymal (70–80%) and renovascular (5–10%) [20]. These may present with malignant hypertension in children. In our study, there was no correlation of the outcome with age, aetiology or severity of hypertension and time to achieve control of blood pressure. Out of 19 children, one had lupus nephritis. RPLS has been reported with lupus nephritis. Two out of 15 patients with RPLS had lupus nephritis in the series by Hinchey et al [1]. In our series, the patient with lupus had a haemorrhagic lesion of the left temporal and right frontal cistern along with white matter change in the occipital region. This spectrum has also been described in a group of uraemic conditions including HUS, hepatorenal syndrome and thrombotic thrombocytopenic purpura [15]. Moreover central nervous system involvement has been known to occur in these patients due to the primary disease per se. The two patients with HUS in our study had occipitoparietal white matter changes which reversed to normal after control of blood pressure. We have also observed haemorrhages in addition to leukoencephalopathic changes in three out of 19 patients. Two out of these three patients have persisting residual leukoencephalopathic changes on follow up scan, despite the size of haemorrhage being reduced. This non-reversibility may be due to the severity of changes which occurred due to hypertension.

The pathophysiology of the reversible posterior leuoencephalopathy syndrome appears to be multifactorial. The mechanism of the syndrome is a brain capillary leak syndrome related to hypertension, fluid retention and possibly the cytotoxic effects of immunosuppressive agents on the vascular endothelium. Severe hypertension per se is perhaps the commonest cause. The sudden elevation in SBP exceeds the autoregulatory capacity of brain vasculature. A region of vasodilatation and vasoconstriction develops especially in the arterial boundary zone and there is breakdown of the blood-brain barrier with transudation of fluid and petechial haemorrhage [21, 22]. In experimental rats that were made suddenly hypertensive, these signs appeared and disappeared suddenly, within hours after relieving hypertension, suggesting the functional vascular changes and vasogenic oedema [23]. There is rapid resolution of clinical signs and symptoms and imaging abnormalities of reversible posterior leuoencephalopathy when blood pressure is lowered in such patients [1]. While the reversibility of such vasogenic oedema is most characteristic, it should be noted that it might result in permanent neurological deficit and cerebral infarct [24]. The predilection for the more posterior involvement in leuoencephalopathy may be due to relatively fewer sympathetic innervations in the posterior cerebral vasculature, which helps to autoregulate the cerebral vessels during acute rise in blood pressure [25]. However, in our study we observed spastic changes in both anterior as well as in posterior circulation suggesting some autoregulatory effect in both these areas. Covarrubias et al [19] have also observed the predilection for posterior circulation territories in RPLS, but not to the exclusion of anterior circulation structures. The involvement of anterior circulation structures such as the frontal (82%) and temporal lobes (91%) was frequently observed in this study [19]. The calcarine and paramedian occipital lobe structure is usually spared, a fact that distinguishes reversible posterior leuoencephalopathy syndrome from bilateral infarction of the posterior cerebral artery territory. Simultaneous bilateral infarction of the posterior cerebral artery territory occurs in patients with embolism to the rostral basilar artery, but with "top of the basilar embolism" the calcarine regions are invariably involved and often there are accompanying thalamic and midbrain infarcts [1, 26].

Similar to our study, involvement of additional areas of the brain in patients with the RPLS, such as the brain stem, cerebellum, basal ganglia and frontal lobes, has also been reported [1–3]. In children, cases of RPLS have been reported consequent upon chemotherapy in patients with leukaemia and lymphoma and the majority of patients recovered after control of hypertension [10–12]. The syndrome should be promptly recognized, since it is reversible and readily treated by controlling blood pressure and discontinuing the offending agents [1]. It has been observed that an incorrect diagnosis of gliomatosis cerebri, progressive multifocal leuoencephalopathy, demyelinating disease or infarction may be advanced on the basis of the MRI finding, if there is an underemphasized aspect of the clinical presentation that is not mentioned to the radiologist. This may result in unnecessary invasive therapy and biopsies [24]. The majority of leuoencephalopathy is reversible within 1–2 weeks. But prolonged seizure, hypertension or both may result in permanent neurological deficit and cerebral infarction. The multiple cerebral infarctions may result in early dementia. A few of them may not recover completely or may have neurodevelopmental sequelae [27]. Kwon et al [27] have shown that one out of 12 patients had small residual haemosiderin deposits on follow up MRI with neurological sequelae.

We conclude that posterior leuoencephalopathy in children with hypertension has a varied clinical and radiological spectrum. The majority of these patients show complete recovery. However, some of them have neurological sequelae especially those with associated haemorrhage on MRI scan. Such children need regular clinical follow up for long-term sequelae. A better understanding of this complex syndrome may obviate unnecessary investigations and allow management of associated problems in prompt and appropriate ways.

Received for publication June 19, 2006. Revision received August 17, 2006. Accepted for publication September 5, 2006.


   References
Top
 Abstract
 Introduction
 Methods and materials
 Results
 Discussion
 References
 

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