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Meenakshi-Sundaram et al. SPECT observations in RPL syndrome

infarction especially in the posterior regions of the There was no word output. Optic fundi revealed
cerebral hemispheres. While such imaging features no papilledema. There were features of grade 3
[2]
have now been well documented, data describing the hypertensive retinopathy. There was right gaze palsy,
functional imaging characteristics in this syndrome right hemiplegia (grade 0/5 over the upper and lower
are rare. [3-6] The pathophysiology of RPL syndrome limbs), bilaterally brisk deep tendon reflexes and
involves cerebral autoregulatory dysfunction. Acute extensor plantar responses.
rise of blood pressure beyond the upper limit of cerebral
autoregulation leads to dilatation of arterioles dilate Investigations revealed: blood urea 29 mg/dL, serum
resulting in cerebral hyperperfusion in a pressure- creatinine 1.6 mg/dL and uric acid 8.8 mg/dL. Urinalysis
passive manner. This leads to breakdown of the blood revealed albuminuria. Hemogram revealed leukocytosis
brain barrier resulting in extravasation of fluid and blood (total leucocyte count 28,500 cells/cu.mm). Abdominal
[7]
products into the brain parenchyma. Early changes ultrasound (done 1 year ago) showed congenital
in neurological diseases can be identified by imaging pelviureteral junction obstruction in the right kidney
regional blood flow which is possible using single with hydronephrotic sac, dilated renal pelvis and
photon emission computerized tomography (SPECT) thinned renal parenchyma and the left kidney showed
imaging which is sensitive to local metabolism and has compensatory hypertrophy. MRI of the brain completed
been utilized in conditions like dementias, epilepsy and on day 2 of the illness revealed multiple lesions that were
traumatic brain injury. SPECT studies may reveal focal hypointense on T1-weighted images, hyperintense on
[8]
areas of hypoperfusion that are discordant with findings T2-weighted and FLAIR images [Figure 1]. The lesions
of MRI or CT. For instance, in traumatic brain injuries involved bilateral cerebellar hemispheres, brainstem,
functional imaging techniques may explain or predict basal ganglia, posterior parieto occipital regions, corona
postinjury neuropsychologic and cognitive deficits that radiata, centrum semiovale and splenium of corpus
are not explained by anatomic abnormalities detected callosum with effacement of ventricular system and
by MRI or CT. SPECT study may thus allow us to sulci. The lesions were moderately bright on diffusion
[9]
understand the clinical correlations of the abnormalities weighted imaging (DWI with b value 600) and lower
detected in routine imaging findings like MRI and such signal in ADC map. Anterior circulation was relatively
correlations pertaining to RPL syndrome are reported spared. MR angiography revealed dolichoectasia
in this communication. with atheromatous dilatation of anterior and posterior
circulation arteries without major vascular occlusion.
CASE REPORT Brain SPECT was performed on the 3rd day of illness
after administration of 20 mCi of Technetium-99m ethyl
A 31-year-old male presented with history of headache cysteinate dimer (99mTc-ECD). Images were acquired
associated with recurrent episodes of vomiting for with a gamma camera, 1 h after tracer administration.
the past 24 h. He developed 2 episodes of right focal Acquired images were then reconstructed in transaxial,
motor to bilateral tonic-clonic seizures 3 h prior to saggital and coronal axes. Images revealed perfusion
admission. Following the seizures he remained in defects involving bilateral basal ganglia, left parieto-
altered sensorium. occipital, right cerebellar and right occipital regions
[Figure 2].
He had a prior medical history of medication-treated
hypertension for the past 4 years. Renal biopsy was Intravenous sodium nitroprusside (0.25 µg/kg/min
obtained 1 year prior to presentation and revealed focal initial dose but then titrated up) was administered for
segmental glomerular sclerosis with multifocal tubular hypertension. Intravenous fosphenytoin (20 mg/kg of
atrophy. He was assessed by nephrologist for the phenytoin equivalent) was given followed by maintenance
same and was then placed on continuous ambulatory phenytoin (5 mg/kg/day) therapy. There were no further
peritoneal dialysis along with antihypertensive therapy recurrences of seizures. His blood pressure gradually
(amlodipine 5 mg/day and prasozin 5 mg/day). He was decreased and oral antihypertensive therapy was
poorly compliant with his anti-hypertensive medicines instituted. His mental status improved by the second
and had discontinued them 1 week prior to this day after admission and limb power was grade 1/5 on
presentation. the 3rd day. The power of his motor movements rapidly
improved subsequently and was grade 5/5 on the
On examination, his recorded vital parameters 5th day after admission and treatment. He remained
were: pulse: 142/min, regular and blood pressure: asymptomatic since the 5th day after admission. At
240/180 mmHg. General physical and cardiorespiratory the time of discharge he was on a combination of
examinations were unremarkable. Neurologically he prasozin 5 mg, clonidine 0.3 mg, labetolol 300 mg and
was drowsy, arousable, but not obeying commands. amlodepine 10 mg/day for control of hypertension.
Neuroimmunology and Neuroinflammation ¦ Volume 4 ¦ February 20, 2017 29