IMAGE OF THE MOMENT

Looking beyond the obvious:
cerebral calcification
Simon W Lines,1 Hawraman Ramadan2
1

Department of Nephrology,
Bradford Teaching Hospitals NHS
Trust, Bradford, UK
2
Department of Neurology &
Stroke Medicine, Bradford
Teaching Hospitals NHS Trust,
Bradford, UK
Correspondence to
Dr Hawraman Ramadan,
Consultant Neurologist and
Stroke Physician, Department of
Neurology & Stroke Medicine,
Bradford Teaching Hospitals NHS
Trust, Bradford, West Yorkshire
BD5 0NA, UK; Hawraman.
Ramadan@bthft.nhs.uk

To cite: Lines SW,
Ramadan H. Pract Neurol
2013;13:386–387.

386

A 63-year-old woman with advanced
chronic kidney disease, diabetes mellitus,
hypertension and peripheral vascular
disease presented with three successive
tonic–clonic seizures. She was obtunded,
with a Glasgow coma scale score of 4/15
but with no lateralising neurological
signs. She had marked renal impairment
(serum creatinine 606 mmol/L (49–90)
and estimated glomerular filtration rate
of 6 mL/min/1.73 m2 (>60)). There was
severe hyperparathyroidism ( parathyroid
hormone 48.8 pmol/L (1.7–7.6)).
CT scan of the head found widespread
infratentorial and supratentorial calcifications, unchanged from a CT scan 2 years
before, and subtle acute subdural and
subarachnoid haemorrhages (figure 1). She
remained comatose and died 14 days later.
It was not clear whether the intracranial haemorrhages were the consequence

of convulsion-related trauma or whether
the haemorrhage caused the seizures.
Intracerebral calcification has a range
of causes and the anatomical distribution provides clues to these (box 1).
Causes include advanced chronic
kidney disease1 where the main drivers
of calcification are phosphate retention
and secondary hyperparathyroidism.2
Intracerebral haemorrhage is more
common in patients with chronic
kidney disease3 reflecting the associated
co-occurrence of diabetes and hypertension and the bleeding diathesis associated with uraemia.4
In this patient, the dramatic and
widespread, though clinically innocuous
cerebral calcifications could distract
the observer from more subtle, yet clinically
more
important
intracranial
haemorrhage.

Figure 1 Plain axial CT scan of brain showing symmetrical calcification of the centrum semiovale
(A–C), basal ganglia (D and E) and cerebellum (F). The thin white arrows show hyperdense right
posterior parafalcine (A and B) and minor left frontoparietal subdural haematoma (A–C) with adjacent
sulcal effacement. Thick white arrow indicates cortical SAH (C). White arrows demonstrate
asymmetrical subcortical (D) and cortical occipital lobes calcification (E).

Lines SW, et al. Pract Neurol 2013;13:386–387. doi:10.1136/practneurol-2013-000591

IMAGE OF THE MOMENT
Box 1 Causes of cerebral calcification: aetiologicalbased classification
Age related/physiological
▸ Choroid plexus, pineal gland, dura, basal ganglia,
cerebellum
Infection
▸ Focal—for example, tuberculosis, cysticercosis
▸ Widespread—for example, chronic viral encaphalitis,
HIV, TORCH
Metabolic abnormalities
▸ Bilateral, symmetrical—for example, hypoparathyroidism/hyperparathyroidism, chronic kidney disease
Vascular disease
▸ Diffuse atherosclerotic large intracranial vessels
▸ Focal—for example, arteriovenous malformation,
cavernoma, aneurysm, chronic subdural haematoma
Inherited syndromes
▸ Bilateral, symmetrical, widepsread—for example,
Fahr’s disease, Gorlin’s syndrome, MELAS syndrome
▸ Focal—for example, tuberous sclerosis, neurofibromatosis, Sturge–Weber syndrome
Neoplasia
▸ Focal—for example, oligodendroglioma, astrocytoma,
meningioma, craniopharyngioma

Acknowledgements The authors thank Ian Melvin for his help
in preparing the images.
Contributors HR had the original idea for the manuscript,
identified the images for publication and helped with the
preparation of the manuscript. SWL wrote the initial draft of
the manuscript and the subsequent modifications and prepared
and labelled the images for publication.
Competing interests None.
Patient consent Obtained.
Provenance and peer review Not commissioned; externally
peer reviewed. This paper was reviewed by Tom Hughes,
Cardiff, UK.

REFERENCES
1 Gionanlis L, Vainas A, Bamihas G, et al. Brain calcinosis in a
dialysis patient with hypoparathyroidism. Nephrol Dial
Transplant Plus 2008;1:36–40.
2 Drueke TB. A clinical approach to the uraemic patient with
extraskeletal calcifications. Nephrol Dial Transplant 1996;11
(Suppl 3):37–42.
3 Chen YC, Su YC, Lee CC, et al. Chronic kidney disease itself is
a causal risk factor for stroke beyond traditional cardiovascular
risk factors: a nationwide cohort study in Taiwan. PLoS ONE
2012;7:e36332.
4 Remmuzzi G. Bleeding in renal failure. Lancet 1988:1:1205–8.

HIV, Human Immunodeficiency Virus; MELAS, Mitochondial
Encephalomyopathy, Lactic Acidosis and Stroke-like episodes; TORCH:
Toxoplasmosis, Other, Rubella, Cytomegalovirus, Herpes simplex virus.

Lines SW, et al. Pract Neurol 2013;13:386–387. doi:10.1136/practneurol-2013-000591

387