J Neurol (1986) 233 : 200-201 Journal of Neurology © Springer-Verlag 1986 Normal mental state despite bilateral pontine tegmental hemorrhage G. H. Sands 1. and R. K. Portenoy 2 i The Department of Neurology, Bronx Municipal Hospital Center, Albert Einstein College of Medicine, Bronx, New York, USA 2 Department of Neurology, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, New York, USA Summary. Alertness was preserved in a 47-year-old hypertensive man who acutely develop headache, cranial nerve abnormalities, weakness and dysmetria. Computerized tomography revealed a bilateral pontine tegmental hemorrhage. This is the first well-documented case of bilateral pontine tegmental hemorrhage with a completely normal mental status. Key words: Cerebral hemorrhage - CT findings - Hypertension - Normal mentation - Pons Large pontine hemorrhages usually present with sudden collapse and coma, though a brief premonitory period of headache, cranial nerve abnormalities, weakness or paresthesiae is often reported [5-8, 11, 15, 16]. The initial examination commonly reveals impaired consciousness, usually coma. Other associated phenomena include respiratory disturbances, fever, pupillary changes, bulbar weakness, ophthalmoparesis and/or gaze palsies with hemiparesis or quadriparesis [5, 6, 10, 16]. We describe a patient who was alert on presentation and had a normal mental status despite sustaining a bilateral pontine tegmental hemorrhage. symmetric, and there was mild rightward deviation of the tongue. He had slight bilateral drift with minimal weakness in both deltoids. His legs were flaccid and he described his severe paraparesis as unchanged. There was severe bilateral dysmetria in the arms, greater in the right than in the left, and rapid movements were markedly impaired. Sensation above a T9 sensory level was normal and the patient confirmed that the severe sensory loss in the legs was unchanged. Reflexes were increased at the biceps and decreased at the knees and ankles. Plantar responses were extensor. There was no evidence of coagulopathy or other abnormalities on laboratory studies, Computerized tomography (CT) revealed on oblong bilateral pontine tegmental hemorrhage, 5 mm in height, which compressed the fourth ventricle (Fig. 1). The patient was treated with corticosteroids, anticonvulsants and antihypertensives. During the 2 days after admis- Case report A 47-year-old hypertensive man complained of the sudden onset of bifrontal throbbing headache, double vision, slurred speech, hearing loss, and perioral numbness. He had a history of paraplegia of 20 years' duration, which occurred immediately following an episode of intravenous drug abuse. On admission, blood pressure was 220/130, respirations were 16 and regular and he was afebrile. He was alert and oriented, would occasionally yawn, and was moderately dysarthric. He followed 3-step commands crossing the midline, could interpret similarities, substract serial 7's, and easily remembered three objects after several minutes. There was no aphasia or apraxia. He had a left abducens paresis and a left gaze palsy, which he could overcome voluntarily. The pupils were 4 mm, round and reactive to light bilaterally. Corneal reflexes were intact and facial sensation was normal. There was a mild facial diparesis and marked bilateral hearing loss, greater in the left ear than in the right. The palate arched normally, the gag was Present address: Division of Neurology, Department of Medicine, Queens Hospital Center Affiliation of Long Island Jewish Medical Center, 82~58164 Street, Jamaica, NY 11432, USA Offprint requests to: Dr. R. K. Portenoy Fig. 1. CT scan showing an area of increased density bilaterally in the pontine tegmentum, representing hemorrhage in the slice shown and in the slices 2-5 mm above and below. The fourth ventricle is compressed 201 sion, he became increasingly lethargic, though he was still able to follow commands. His dysarthria, facial diparesis and arm weakness worsened. He developed a skew deviation with his right eye hypertropic, upgaze nystagmus, a right internuclear ophthalmoplegia and increased tone in his legs. Worsening lethary and tachypnea necessitated intubation and a pneumonia was treated. With extubation 1 week later the patient was alert and had a mental status unchanged from admission. In addition to his other findings, he was hypophonic and at times aphonic. He had also developed decreased tongue motion, increased dysphagia and a dominished gag reflex. His course became complicated by recurrent and persistent pneumonia, urinary tract infection, mild hepatitis, and anemia. His neurologic state remained unchanged for several weeks, except for resolution of the internuclear ophthalmoplegia. After reintubation for worsening pneumonia, he remained alert and capable of following complex commands. Despite antibiotics and respiratory support, he developed progressive hypoxemia and died 1 month after admission. Permission for autopsy was refused. level of consciousness and the extent of the lesion across the midline of the tegmentum. All nine patients with bilateral tegmental involvement were unresponsive. They also noted that cats with bilateral mesencephalic transections go into a sleeplike state, while those with lesions more caudal than midpons have normal alertness. In man, alert behavior appears to be dependent on the intactness of structures in the rostral pontine tegmentum [4]. The more caudal pontine tegmental involvement, demonstrated both clinically and radiographically in our patient, may explain the preservation of his normal mental state. Our patient is the first well-documented case of bilateral pontine tegmental hemorrhage presenting with a completely normal mental status. As experience with CT scanning expands, it is clear, as Freeman et al. [9] suggested, that lesions in the pons produce various syndromes according to the particular location of the damage. Gowers, as quoted by Silverstein [15], stated in 1888 that in pontine hemorrhage "initial loss of consciousness may be present or absent just as in hemorrhage elsewhere." The present case illustrates that this applies to the pontine tegmentum as well. Discussion References There have been rare reports of patients with bilateral pontine tegmental hemorrhages who were alert on presentation. Epstein [6] reported two patients (cases 6 and 7) who were conscious. No details of the mental status exam are given beyond the fact that one patient was "unable to speak but able to follow directions." A t autopsy both were found to have hemorrhage throughout most of the pons. Other cases in which patients were alert had lesions limited to one side of the pons. Muller et al. [13] described a patient with a CT-documented right pontine hemorrhage involving both the basis pontis and tegmentum, who was "awake and collaborative" on initial examination. Burns et al. [2] reported two patients with pontine tegmental hemorrhages, who had intact mental status. Although we know the first patient had a pontine tegmental hemorrhage, we are unable to ascertain whether there is unilateral or bilateral involvement with the description given. The second patient had a dorsolateral mesencephalic hemorrhage demonstrated by CT. Bressman and Kushner [1] reviewed 12 cases of brainstem hemorrhage; they found that all four patients with retained consciousness had unilateral lesions. Their recent review of the clinical symptoms of pontine hemorrhage did not include any patients with bilateral tegmental involvement and a normal mental status [12]. There have been several reports of patients who were lethargic or stuporous, but not comatose, on presentation. Unilateral lesions were usually found in these cases as well. Silverstain [15], for example, described such a mild alteration of consciousness in lesions of the lateral tegmentum and noted that more central lesions typically produced marked impairment. Coma did not occur in 9 of 10 cases of lateral tegmental hemorrhage reported by Caplan and Goodwin [3]. A single patient has been described with bilateral tegmental hemorrhage who was "acutely lethargic but was aroused easily by normal conversational tone" and oriented to time, not place I14]. Chase et al. [4[ reported an autopsy series of pontine vascular lesions, which showed a direct relationship between the 1. Bressman S, Kushner M (1981) Some natural history of brainstem hemorrhage diagnosed during life. Neurology (NY) 31 : 92 2. Burns J, Lisak R, Schut L, Silberberg D (1980) Recovery following brainstem hemorrhage. Ann Neurol 7:183-184 3. Caplan LR, Goodwin JA (1982) Lateral tegmental brainstem hemorrhages. Neurology (NY) 32 : 252-260 4. Chase TN, Moretti L, Prensky AL (1968) Clinical and electroencephalographic manifestations of vascular lesions of the pons. Neurology (Minneap) 18: 357-368 5. Dinsdale HB (1964) Spontaneous hemorrhage in the posterior fossa. Arch Neurol 10:200-217 6. Epstein AW (1951) Primary massive pontine hemorrhage. J Neuropathol Exp Neurol 10: 426--448 7. Fang HCH, Foley JM (1954) Hypertensive hemorrhages of the pons and cerebellum. Trans Am Neurol Assoc 79: 126-130 8. Fisher CM (1961) Clinical syndromes in cerebral hemorrhage. In: Fields W (ed) Pathogenesis and treatment of cerebrovascular disease. 7th Annual Scientific Meeting of the Houston Neurological Society, Texas Medical Center, Houston, Texas. Charles C. Thomas, Springfield, pp 318-342 9. Freeman W, Ammerman H, Stanley M (1943) Syndrome of the pontile tcgmentum, Foville's syndrome: report of three cases. Arch Neurol Psychiatry 50:462--471 10. Goto N, Kaneko M, Hasaka Y, Koga H (1980) Primary pontine hemorrhage: clinicopathologicalcorrelations. Stroke 11 : 84-90 11. Kase CS, Maulsby GO, Mohr JP (1980) Partial pontine hematomas. Neurology (NY) 30: 652-655 12. Kushner M, Bressman S (1985) The clinical manifestations of pontine hemorrhage. Neurology (Cleveland) 35 : 637-643 13. Muller H, Wurthrich R, Wiggli K, Hunig R, Elke M (1975) The contribution of computerized axial tomography to the diagnosis of cerebellar and pontine hematomas. Stroke 6 : 467-475 14. Payne H, Maravilla K, Levinstone A, Heuter J, Tindall TR (1978) Recovery from primary pontine hemorrhage. Ann Neurol 4: 557558 15. Silverstein AJ (1972) Primary pontine hemorrhage. In: Vinken PJ, Bruyn GW (eds) Handbook of clinical neurology, vol XII. Vascular diseases of the nervous system, part II. North Holland, Amsterdam, pp 37-53 16. Steegman AT (1951) Primary pontine hemorrhage. J Nerv Ment Dis 114: 35-65 Received August 13, 1985 / Accepted November 8, 1985