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LETTERS Potassium of 3.4 Mmol/L 820 J Neurol Neurosurg Psychiatry 2003;74:820–826 J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.74.6.823 on 1 June 2003. Downloaded from sodium concentration of 136 mmol/l and The two patients presented here showed LETTERS potassium of 3.4 mmol/l. The serum phos- aclose temporal association between severe phate concentration was profoundly low at hypophosphataemia and the development of 0.13 mmol/l. T2 weighted and FLAIR se- CPM. Both patients abused alcohol, and the Central pontine myelinolysis quence MRI done three days after admission first patient had moderate hyponatraemia temporally related to showed abnormal signal within the central with hypokalaemia. They may therefore have brain stem suggestive of CPM (fig 1). hypophosphataemia been particularly susceptible to CPM for a She was treated with oral thiamine, multi- variety of reasons. It is possible, however, that Central pontine myelinolysis (CPM) is known vitamins, and minerals including phosphate. severe hypophosphataemia adversely affected to be associated with the rapid correction of She made a rapid improvement such that her the Na+/K+-ATPase pump and finally trig- severe hyponatraemia. However, there have dysarthria had resolved and gait improved gered apoptosis and CPM. The temporal been case reports of CPM occurring in sufficiently for her to be discharged 11 days association of neurological deterioration with 1 after admission. normonatraemic patients. Here we describe the rapid correction of profound hypophos- two patients in whom chronic alcohol abuse Comment phataemia in case 1 is unlikely to relate to led to profound hypophosphataemia that was The pathophysiology of CPM is not well osmotic stress in view of the small contribu- closely temporally related to the development understood. Rapid correction of severe hypo- tion of phosphate towards total osmolarity. of CPM. natraemia is frequently implicated as a causa- The rapid change in plasma phosphate may, however, increase cellular stress, contributing Case 1 tive factor, but CPM has been reported in the presence of normonatraemia,1 hypokalemia,2 to eventual apoptosis. A 29 year old woman was admitted for investi- and hypophosphataemia.3 In these cases a Both patients described here made good gation of painless jaundice of 10 days’ dura- hypothesis based on osmotic trauma must be recoveries with phosphate replacement and tion. She had consumed 100–140 units of questioned. supportive care. This suggests that wide- alcohol a week for the preceding 18 months Recently an apoptotic hypothesis has been spread apoptosis had not occurred. In these and had been noted to have mildly deranged proposed.4 It is suggested that a depletion of patients the speed and degree of recovery serum transaminase levels one year previously. the energy supply to glial cells might limit the might reflect the resolution of pontine On admission she was fully oriented with function of their Na+/K+-ATPase pumps. This oedema that could accompany less wide- normal speech and gait. She had a mild could reduce their ability to adapt to relatively spread or incomplete apoptosis. postural tremor but no asterixis. A plasma minor osmotic stress caused by small changes There are useful practical conclusions to be biochemical profile showed her sodium to be in serum sodium concentration, and ulti- drawn from the observed association of CPM 122 mmol/l, potassium 2.1 mmol/l, and urea mately lead to apoptosis. A preliminary study with hypophosphataemia. First, one must µ 5.9 mmol/l. Serum creatinine was 182 mol/l, of necropsy material from five cases of CPM suspect the diagnosis of CPM in susceptible phosphate 0.65 mmol/l, magnesium 0.59 compared with controls has provided some patients even without “typical” electrolyte mmol/l, and total corrected calcium 2.18 support for this theory. Using immunohisto- abnormalities. Second, as severe hypophos- mmol/l. She was immediately given potas- chemistry, an imbalance was shown between phataemia in itself has been correlated with proapoptotic and antiapoptotic factors in glial 6 sium and magnesium supplements, chlo- increased mortality it would seem prudent to rdiazepoxide, and intravenous vitamins in- cells with the appearance of oligodendro- 5 check and treat low serum phosphate concen- cluding vitamin K and thiamine. cytes. Furthermore the serum sodium con- centrations in two of the patients remained trations in susceptible patients. This particu- Three days after admission she developed a larly refers to alcohol abusers or malnour- Staph aureus septicaemia secondary to a normal from the onset of symptoms to the time of death. ished patients treated with intravenous peripheral venous cannula infection. This glucose, diuretics, and steroids which may required treatment with intravenous cefuro- lower serum phosphate concentrations. xime and flucloxacillin. She subsequently became drowsy and by day 10 had developed A W Michell, D J Burn, P J Reading a severe spastic dysarthria and profound Regional Neurosciences Centre, spastic tetraparesis. There was a bilateral Newcastle-upon-Tyne, UK lower motor neurone pattern of facial weak- ness and gaze evoked nystagmus. The clinical Correspondence to: Dr Michell; suspicion of CPM was supported by magnetic [email protected] http://jnnp.bmj.com/ resonance imaging of the brain, which References showed symmetrical signal hyperintensity in 1 Bernsen HJJA, Prick MJJ. Improvement of the pons on T2 weighted images, as well as central pontine myelinolysis as demonstrated generalised cerebral atrophy. by repeated magnetic resonance imaging in a A review of the biochemistry results during patient without evidence of hyponatremia. her admission showed that the maximum Acta Neurol Belg 1999;99:189–93. increase in serum sodium concentration over a 2 Bähr M, Sommer N, Petersen D, et al. Central 24 hour period was only 7 mmol/l (from 123 to pontine myelinolysis associated with low 130 mmol/l). Potassium and magnesium con- potassium levels in alcoholism. J Neurol 1990;237:275–6. centrations were corrected to the lower end of on September 28, 2021 by guest. Protected copyright. 3 De Broucker T, Rueff B, Hammel P, et al. their normal ranges. However, she developed L’hypophosphorémie: cause possible de profound hypophosphataemia (0.16 mmol/l at myélinolyse centropontine. Presse Med nadir) which was rapidly corrected to 0.8 1989;18:1166. mmol/l within 72 hours. The rapid rise in 4 Ashrafian H, Davey P. A review of the plasma phosphate coincided with the onset of causes of central pontine myelinolysis: yet the patient’s neurological deterioration. With another apoptotic illness? Eur J Neurol supportive care she made a gradual recovery 2001;8:103–9. DeLuca GC such that two months after admission she was 5 , Nagy Z, Esiri MM, et al. Evidence for a role for apoptosis in central safe to be discharged, with only a mild residual pontine myelinolysis. Acta Neuropathol left hemiparesis and slight spastic dysarthria, 2002:103:590–8. which were improving. 6 Halevy J, Bulvik S. Severe hypophosphatemia in hospitalized patients. Arch Intern Med Case 2 1988;148:153–5. A 44 year old woman was admitted with a three day history of progressive dysarthria, seven days of difficulty in walking, and Spastic movement disorder: dysaesthesia affecting all four limbs and the what is the impact of research perioral region. She had consumed at least 80 on clinical practice? units of alcohol a week for several months before presentation. Figure 1 Coronal FLAIR magnetic One expects that convincing research results Examination on admission revealed a mild resonance image (MRI) (A) and axial T2 would have an impact on clinical practice. tetraparesis, dysarthria, and subjective sen- weighted MRI (B) from case 2, showing high However, whether or not a new concept sory loss in both legs and the left arm. Her signal within the pons consistent with central becomes transferred to an application in admission blood profile revealed a plasma pontine myelinosis. clinical practice is dependent on the medical www.jnnp.com J Neurol Neurosurg Psychiatry 2003;74:820–826 821 J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.74.6.823 on 1 June 2003. Downloaded from field and on the therapeutic consequences. The following factors may contribute to the 8 Ibrahim IK, Berger W, Trippel M, et al. The issue discussed here concerns spasticity, a persistence of some old fashioned concepts in Stretch-induced electromyographic activity and common motor disorder in, for example, clinical neurology: torque in spastic elbow muscles. Brain patients who have had a stroke or a spinal 1993;116:972–89. • The old concept was simple to understand O’Dwyer NJ cord injury. 9 , Ada L, Neilson PD. Spasticity and had a clear therapeutic consequence: and muscle contracture following stroke. Brain The traditional concept the prescription of antispastic drugs. It is 1996;119:1737–49. seemingly logical that exaggerated reflexes 10 O’Dwyer NJ, Ada L. Reflex hyperexcitability Over many years it was widely accepted that and muscle contracture in relation to spastic spasticity consists of muscle hypertonia (that cause muscle hypertonia. The new concept hypertonia. Curr Opin Neurol is, “a velocity dependent resistance of a mus- is more complex and its implications—that 1996;9:451–5. cle to stretch”1) caused by exaggerated re- antispastic drugs should not generally be 11 Powers RK, Marder-Meyer J, Rymer WZ. flexes, leading to the spastic movement used—make the doctor somewhat re- Quantitative relations between hypertonia and disorder.2 This concept was based on animal sourceless. stretch reflex threshold in spastic hemiparesis. experiments (for example, in the decerebrate Ann Neurol 1988;23:115–24. cat3) and on the physical signs evident on • It is not rewarding for a neurologist to take 12 Hiersemenzel LP, Curt A, Dietz V. From clinical examination at the bedside. Conse- care of patients after a stroke and to have to spinal shock to spasticity. Neuronal explain that there are limited therapeutic adaptations to spinal cord injury.
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