Journal of

J Neurol (1985) 232 : 58-59

Neurology
© Springer-Verlag 1985

Focal luxury perfusion with an early-filling vein
in relation to neurological symptoms evoked by heat
S. Yorifuji 1, M. Takahashi 1, S. Ogasahara 1, Y. Nakamura 1, T. Hazama 1, M. Mitomo 2, and S. Tarui 1

I Second Department of Internal Medicine and 2 Department of Radiology, Osaka University Medical School,
1-1-50 Fukushima, Fukushima-ku, 553 Osaka, Japan

Summary. A 50-year-old man with a 1-year history of transient attacks of left total hemiparesis was admitted to hospital
with a complaint of increasing frequency of attacks. Minimal
or moderate left hemiparesis was elicited by elevation of
environmental temperature when taking a hot bath or a hot
shower. Right carotid angiography revealed an early-filling
vein near the right central sulcus. A n increase of focal luxury
perfusion by elevation of body temperature seemed to cause
relative ischaemia in this paracentral gyrus.
Key words: Transient ischaemic attack - Luxury perfusion Body temperature

Introduction

It is well known that neurological deficit is elicited by elevation of environmental temperature in some patients with
multiple sclerosis [2, 4, 7]. Such a phenomenon is rarely observed in patients with other diseases [4]. We report a patient
with small focal luxury perfusion in the cortical motor area
showing contralateral hemiparesis during the elevation of
environmental temperature.

Case report

On 6 January 1982, a 50-year-old man first had an attack of
left total hemiparesis; this neurological deficit disappeared
completely 2 days later. Plain computed tomography of the
brain revealed no abnormality. Six months after the first
attack he was admitted with increasing frequency of transient
attacks of minimal left hemiparesis, each continuing for about
2 h. His transient neurological deficit was sometimes noted
three times per day and usually occurred when taking a hot
bath or shower. He therefore usually took a bath or a shower
with lukewarm water. Examination revealed a mild cardiac
systolic murmur, suggesting a congenital atrial septal defect.
His blood pressure was 160/70mmHg with no orthostatic
hypotensin and his pulse rate was 88/min and regular. Neurological examination showed slight shallowness of the left nasolabial fold. A "hot bath test" was refused by the patient. However, a "hot shower test" gave a positive result; several
Offprint requests to: Shiro Yorifuji, MD (address see above)

minutes after taking a hot shower, he showed minimal left
total hemiparesis and increased muscle stretch reflex in the
left upper and lower extremities. The grip power of his left
hand decreased from 55 kg to 11 kg. Dysaesthesia and hypalgesia in the left face and left upper extremity were also
noted. Systemic blood pressure did not change during this
test. These neurological signs disappeared several hours after
the hot shower. Examination by cardiac catheterization
showed passage of the catheter across the atrial defect, but no
right-to-left shunt through an atrial septal defect. Echocardiogram revealed no abnormality other than the atrial septal
defect. Laboratory examinations, including cerebrospinal
fluid, gave no abnormal results. Electroencephalogram was
normal. CT scan of the brain was also normal, but in the right
carotid angiogram an early-filling vein was seen near the right
paracentral sulcus (during a non-symptomatic period; Fig. 1).
Anticoagulant therapy with aspirin or medication with vasodilators did not decrease the frequency of ischaemic attacks.

Discussion

In 1937, Simons [7] originally reported that heat and cold
might influence certain symptoms in patients with multiple
sclerosis. In 1951, Guthrie [2] reported that elevated environmental temperature may induce changes in visual and motor
function in patients with multiple sclerosis, suggesting that this
phenomenon may be due to changes in blood circulation in
the central nervous system during heating. Many authors have
reported similar phenomena in patients with multiple sclerosis
[3]. In 1973, Rasminsky [6] reported that elevation of temperature caused reversible conduction block at identifiable
internodes of experimentally demyelinated rat ventral root
fibres. He suggested that neurological deficit in patients with
multiple sclerosis during elevation of environmental temperature may be due to the direct effect of elevated temperature
on the affected demyelinated fibres [4]. In a similar way, intermittent claudication during exertion is induced in some
patients with arteriovenous malformation [1]. The mechanism
of this phenomenon is thought to be stealing of arterial blood
flow to other regions [5-7]. In this report we describe a patient
with intracerebral small localized luxury perfusion in the right
paracentral sulcus, showing focal neurological deficits corresponding to the affected area, after a hot shower. The mechanism that causes this phenomenon may be similar to that in

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Fig. 1. Late arterial phase of the fight carotid angiogram showing early-filling vein (arrow) in the region of the right central sulcus

patients with arteriovenous malformation. Increased luxury
perfusion by elevation of environmental t e m p e r a t u r e must
cause relative ischaemia of the surrounding cerebral cortex.
Presumably this lesion is not congenital because no neurological deficit was found before the first attack at the age of
49 years. The reason for the first ischaemic attack is uncertain.
W e consider that it might have been caused by embolism
because this patient had a congenital cardiac anomaly, with
no arteriosclerotic change, confirmed by angiography. In
general, a capillary blush and an early-filling vein have b e e n
detected by angiography in the acute phase in 36% of patients
with recanalization of occluded arteries and in cerebral
neoplasms [8-20]. Neither intracranial neoplasm nor new
attack of cerebral infarction were present in this case. Thus we
consider that this lesion may have persisted after the first
hemiplegic attack in the region of the occluded and recanalized artery. T h e r e seems to have b e e n no previous report of a
patient whose neurological instability during the elevation of
environmental t e m p e r a t u r e was caused by the focal luxury
perfusion in the cerebral cortex.

2. Guthrie TC (1951) Visual and motor changes in patients with
multiple sclerosis. A result of induced changes in environmental
temperature. Arch Neurol Psychiatry 65 : 437-451
3. Irino T, Taneda M, Minami T (1977) Angiographic manifestations
on post recanalized cerebral infarction. Neurology (Minneap)
27 : 471-475
4. Kurtzke JF (1970) Clinical manifestations of multiple sclerosis. In:
Vinken P J, Bruyn W (eds) Handbook of clinical neurology, vol 9.
North-Holland, Amsterdam Oxford New York, pp 161-216
5. Mossy J (1976) Vascular diseases of the spinal cord. In: Baker
AB, Baker LH (eds) Clinical neurology, vol 3. Haper & Row,
Hagerstown, p 11
6. Rasminsky M (1973) The effects of temperature of conduction in
demyelinated single nerve fibres. Arch Neurol 28 : 287-292
7. Simons DJ (1937) A note on the effect of heat and cold upon
certain symptoms of multiple sclerosis. Bull Neurol Inst NY
6: 385-386
8. Taveras JM, Gilson JM, Davis DO, Kilgore B, Rumbaugh CL
(1969) Angiography in cerebral infarction. Radiology 93 : 549-558
9. Taveras JM, Wood FH (1976) Carotid angiography. In: Taveras
JM, Wood FH (eds) Diagnostic neuroradiology, 2nd edn. Williams and Wilkins, Baltimore, p 650
10. Waxman SG (1981) Clinicopathological correlations in multiple
sclerosis and related diseases. Adv Neurol 31 : 169-182

References
1. Beraud R (1972) Vascular malformations of the spinal cord. In:
Vinken PJ, Bruyn W (eds) Handbook of clinical neurology, vol
12. North-Holland, Amsterdam Oxford New York, pp 548-555

Received August 6, 1984 / Accepted December 3, 1984