Indian Journal of Nuclear Medicine

: 2017  |  Volume : 32  |  Issue : 3  |  Page : 250--251

Cerebral spinal fluid cisternography in normal pressure hydrocephalus of the elderly

Shoukat Hussain Khan, Tanveer Ahmad Rather, Sayantani Sinha 
 Department of Nuclear Medicine, Sher-I-Kashmir Institute of Medical Sciences, Srinagar, Jammu and Kashmir, India

Correspondence Address:
Shoukat Hussain Khan
Department of Nuclear Medicine, Sher-I-Kashmir Institute of Medical Sciences, Srinagar - 190 011, Jammu and Kashmir

How to cite this article:
Khan SH, Rather TA, Sinha S. Cerebral spinal fluid cisternography in normal pressure hydrocephalus of the elderly.Indian J Nucl Med 2017;32:250-251

How to cite this URL:
Khan SH, Rather TA, Sinha S. Cerebral spinal fluid cisternography in normal pressure hydrocephalus of the elderly. Indian J Nucl Med [serial online] 2017 [cited 2022 Oct 3 ];32:250-251
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A 70-year-old woman with type 2 diabetes mellitus presented with symptoms of urinary incontinence, mild cognitive impairment, and gait disturbance for 1 month was subjected to cerebral spinal fluid (CSF) cisternography. On clinical examination, the patient was irritable with a Glasgow coma scale score of 14. Her magnetic resonance imaging (MRI) head revealed dilatation of lateral ventricles with atrophy of frontotemporal regions and gross widening of extracerebral CSF spaces on T2-weighted axial image [Figure 1]. There appeared to be a diagnostic dilemma between normal pressure hydrocephalus (NPH) and an ex vacuo dilatation due to corticocentral atrophy. Technetium (Tc)-99m diethylenetriaminepentaacetic acid (DTPA) (37 MBq) was administered intrathecally through a lumbar puncture. The spectrum of CSF flow patterns imaged on a gamma camera fitted with low energy all-purpose parallel hole collimator traced the thecal ascend of radiotracer in the 30 min image, and at 90 min, the radiotracer was visualized in the basilar cisterns, Sylvian cisterns and the lateral ventricles [Figure 2]. In the delayed 24 h image, persistent ventricular activity with scanty migration over the cerebral convexities was seen [Figure 2]. This pattern of persistent ventricular activity with inadequate migration or no activity over cerebral convexities (Type-IV cisternographic pattern) seen in patients of communicating NPH is who are likely to benefit from a therapeutic CSF shunting procedure.[1]{Figure 1}{Figure 2}

Hydrocephalus in elderly patients may be due to NPH which improves with symptomatic relief after a CSF shunting procedure. However, differentiating NPH from a secondary ventricular dilatation in cerebral cortical atrophy may be difficult on the standard radiological imaging such as computed tomography (CT) and MRI. The spectrum of radionuclide CSF flow images provides useful information of CSF dynamics which is of immense utility in differentiating NPH from cortical atrophy and also aids in deciding a therapeutic CSF shunting procedure in patients of NPH. However, after the advent of CT and MRI, radionuclide cisternography is used sparingly for the evaluation of CSF flow dynamics.[2],[3],[4] CSF cisternography is usually performed after intrathecal injection of indium-111 DTPA (250 μCi). A half-life of 67 h offers advantages in terms of good quality delayed imaging. Spinal cord receives the highest dose of 0.95 mGy/MBq with an effective dose of 0.14 mSv/MBq. Intrathecal Tc-99m DTPA commonly used in detection and localization of CSF leaks can be used as an alternate radiopharmaceutical in an intrathecal dose of 0.5–1 mCi (18.5–37 MBq) for CSF flow cisternography.[5] The images are of interpretable quality with a considerably lesser spinal cord dose of 0.046 mGy/MBq with an effective dose of 0.011 mSv/MBq.[6] DTPA owing to its nonlipid solubility, high-molecular weight, and being neither metabolized nor absorbed transependymally remains in the CSF throughout the imaging thus making it a very suitable agents for radionuclide cisternography after labeling it with indium-111 or Tc-99m. Radionuclide cisternography continues to retain its usefulness in differentiating NPH from cerebral cortical atrophy and in deciding a therapeutic CSF shunt procedure in patients with NPH.

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