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Sustained downgaze in coma after cardiac arrest
  1. K JOHKURA
  1. Department of Neurology, Medical Center, Yokohama City University, 4–57 Urafune-cho, Minami-ku, Yokohama 232–0024, Japan
  2. Department of Neurology, Hiratsukakyosai Hospital, Hiratsuka, Japan
  3. Department of Neurology, Yokohama City University School of Medicine, Yokohama, Japan
  1. Dr K Johkura kjm0502{at}urahp.yokohama-cu.ac.jp
  1. A KOMIYAMA
  1. Department of Neurology, Medical Center, Yokohama City University, 4–57 Urafune-cho, Minami-ku, Yokohama 232–0024, Japan
  2. Department of Neurology, Hiratsukakyosai Hospital, Hiratsuka, Japan
  3. Department of Neurology, Yokohama City University School of Medicine, Yokohama, Japan
  1. Dr K Johkura kjm0502{at}urahp.yokohama-cu.ac.jp
  1. Y KUROIWA
  1. Department of Neurology, Medical Center, Yokohama City University, 4–57 Urafune-cho, Minami-ku, Yokohama 232–0024, Japan
  2. Department of Neurology, Hiratsukakyosai Hospital, Hiratsuka, Japan
  3. Department of Neurology, Yokohama City University School of Medicine, Yokohama, Japan
  1. Dr K Johkura kjm0502{at}urahp.yokohama-cu.ac.jp

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Sustained downgaze eye deviation is occasionally associated with lesions affecting the dorsal midbrain, usually thalamic haemorrhage. In stuporous or comatose patients, however, this downgaze does not necessarily indicate structural pretectal damage.1 Subarachnoid haemorrhage, seizure, hepatic failure, hypoglycaemia, intoxication with sedative drugs, and hypoxic encephalopathy can cause this eye sign in comatose patients.1 We report on three comatose patients who showed sustained downgaze after cardiac arrest. The paper concentrates particularly on the temporal neuro-ophthalmological profile.

Between January and December 1998 we examined three patients with sustained downgaze. All three patients underwent brain CT and EEG while sustained downgaze was present (table 1). Brain MRI was performed only in patient 2, 2 weeks after admission. All patients were in a comatose state after cardiac arrest, responding only to painful stimuli. Deep tendon reflexes were slightly increased in patient 1 but normal in patients 2 and 3. Flexor plantar reflexes were elicited in all patients. Cardiac arrest was due to anaphylaxis in patient 1, cardiomyositis in patient 2, and ventricular fibrillation in patient 3. Arrest time ranged from 10 to 30 minutes before resuscitation. All patients had not received any sedative drugs.

Table 1

Clinical data of the patients

Sustained downgaze deviation was recognised in each patient when the eyelids were raised after a period of 1 to 4 days, when the immediate post-resuscitation threat of death had subsided. Horizontal oculocephalic responses were present in all patients, and the eyes could be driven upward with vertical oculocephalic manoeuvres. The pupils were normal in size and showed normal reactions to light. In patient 1, high frequency horizontal head shaking was followed by transient conjugate upward ocular deviation. After a few seconds of horizontal head shaking at a frequency of 2 Hz, the eyes moved slowly upwards, remained there for a few seconds, and lowered slowly. This phenomenon was recognised only while sustained downgaze was evident. This upward ocular deviation could not be elicited in the other two patients. In patient 2, smooth and then saccadic ping-pong gaze2 was detected transiently 2 days after admission; the ping-pong gaze disappeared when the eyes began to deviate downward 4 days after admission. Marked rigidity and dorsiflexion of the neck and trunk were associated with sustained downgaze in this patient; rigidity of the limbs was mild. This abnormal rigidity and dorsiflexion resolved with the disappearance of the sustained downgaze. Muscle tonus of the other two patients was slightly decreased.

Brain CT findings in all patients and MRI findings in patient 2 seemed normal. An EEG showed a generalised delta rhythm intermingled with theta waves in patient 1, low voltage fast activity in patient 2, and suppression burst in patient 3. The sustained downgaze disappeared within 1 week in all patients, but all have remained in a persistent vegetative state.

Our three patients experienced acute onset coma as a result of diffuse CNS damage after cardiac arrest. The EEG results in our patients suggested the existence of diffuse, severe brain damage. The ping-pong gaze seen in patient 2 also implied severe bilateral cerebral damage.2 The sustained downgaze appeared in our patients 1 to 4 days after resuscitation. That was also the time at which patients were emerging from the most critical postevent stage. In a previously reported patient with hypoxic encephalopathy, downgaze was recognised after 2 weeks of coma.1 These findings suggest that sustained downgaze is not an eye sign in dying patients but that it appears in patients reaching an early recuperation stage. This notion is supported by our finding that the ping-pong gaze changed from a smooth to a saccadic pattern before appearance of the sustained downgaze in one patient; such transition suggests clinical improvement.2 It remained unclear which function might have improved as a prerequisite for the sustained downgaze.

Keane reported sustained upgaze deviation after cardiac arrest.3 Our present findings indicate that sustained downgaze may also be associated with hypoxic encephalopathy after cardiac arrest. The most striking difference between the sustained upgaze reported by Keane3 and sustained downgaze is the time of appearance; sustained upgaze appears immediately after cardiac arrest whereas sustained downgaze is recognised after a few days. The temporal relation between the upgaze or downgaze and ping-pong gaze2 confirms this difference as ping-pong gaze is reported to appear after resolution of sustained upgaze,3whereas it preceded sustained downgaze in our patient. Keane speculated that the sustained upgaze deviation after cardiac arrest resulted from hypoxic cerebellar damage due to diffuse CNS hypoperfusion.3 The possible mechanism of upgaze deviation with cerebellar damage is a disinhibition of anterior canal projections for upward vestibulo-ocular reflex caused by bilateral floccular dysfunction.4 When this has recovered, the subsiding depression of mesencephalic neuronal circuits for upgaze might explain subsequent downgaze deviation. Sustained upgaze may be a direct result of diffuse CNS hypoperfusion in which the cerebellum is severely impaired,3 and sustained downgaze may be a result of partial recovery from diffuse, severe cerebral depression. This is consistent with the fact that all our patients with sustained downgaze lived, although they remained in a persistent vegetative state, whereas almost all reported patients with sustained upgaze died.3

One of our patients showed transient upward eye deviation after high frequency horizontal head shaking during the period of sustained downgaze. Walker and Zee5 described high frequency horizontal head shaking as transiently leading to and increasing upward slow eye movements that result in downbeat nystagmus in patients with cerebellar degeneration. Thus, the upward eye deviation after horizontal head shaking in our patient may imply severe underlying cerebellar damage.

Our second patient had marked rigidity and dorsiflexion of the neck and trunk during the period of sustained downgaze. Rigidity and dorsiflexion are typical symptoms of progressive supranuclear palsy, in which the midbrain tegmentum is severely damaged.6Bilateral lesions of the interstitial nucleus of Cajal, which lies in the midbrain tegmentum, have been reported to result in dorsiflexion of the neck similar to that seen in progressive supranuclear palsy.6 It could be that dorsal midbrain involvement was responsible for our patient's rigidity and dorsiflexion.

More than one anatomical site or physiological mechanism may well be involved in forced downgaze in comatose patients after cardiac arrest, and the mechanistic details of this state are still unclear. However, it is important to recognise that sustained downgaze can appear transiently a few days after cardiac arrest and resuscitation.

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