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Golf ball epilepsy
  1. DAVID CHADWICK,
  2. DANIELA B CLEAR,
  3. PAUL ELDRIDGE,
  4. CONNOR MALUCCI
  1. The Walton Centre for Neurology and Neurosurgery, Lower Lane, Liverpool L9 7LJ, UK
  1. Professor D Chadwick, University Department of Neurological Science, The Walton Centre for Neurology and Neurosurgery, Lower Lane, Liverpool L9 7LJ, UK

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(A) CT showing acute extradural haematoma in patient 1. (B) CT 5 days after A showing persisting cortical abnormality after evacuation of extradural haematoma. (C) CT demonstrating minor depressed skull fracture at site of impact. (D) CT showing late cortical changes at presumed site of impact 4 years after injury.

Blunt head injuries may cause epilepsy. We present the cases of four young people whose heads were all subject to contact with golf balls travelling at speed. Each had post-traumatic seizures, three early and one late, despite the apparent absence of post-traumatic amnesia. Although many patients who develop epilepsy recall some type of head injury preceding their first seizure, post-traumatic epilepsy probably accounts for less than 5% of all the epilepsies.1 There is good evidence that the risk of post-traumatic epilepsy increases with the severity of the injury. Thus, Jennett2 identified the presence of intracranial haemorrhage, dural laceration, and early post-traumatic seizures as the chief risk factors for late post-traumatic epilepsy. Annegerset al also emphasised that in the absence of a post-traumatic amnesia of 30 minutes or greater, there was no significant increased risk for the development of post-traumatic epilepsy.3

From a practical point of view and for medicolegal purposes, it is necessary to decide if a seizure is post-traumatic. As a general rule it may be stated that if the person concerned does not give a history of a post-traumatic amnesia lasting for a significant period of time (an hour or more), and there is no history of a compound or depressed fracture with dural tear, it is reasonable to exclude the possibility that the epilepsy is post-traumatic. However, it is worth noting that this view is based on Jennett's work and precedes CT. There is no good evidence from a large series to indicate whether findings on acute imaging add anything to the prediction of post-traumatic epilepsy.

Four examples of acute symptomatic seizures and epilepsy developing after head injuries with golf balls are described, which seem to be an exception to these clinical rules.

An 11 year old boy was struck on the right temple by a golf ball resulting in right frontal scalp contusion. His consciousness was not impaired until about 3 hours later when he became drowsy and had two focal motor seizures affecting the left arm. He was intubated and ventilated. A head CT showed a right frontal extradural haematoma with no skull fracture (figure A). The haematoma was evacuated (figure B). He was woken and extubated the next day and was discharged without neurological impairment two days later on phenytoin. No further follow up is yet available.

A 16 year old boy, who was a keen golfer with a single figure handicap, was struck on the head by a golf ball which rebounded several yards after striking him on the forehead. He experienced local pain, bruising, and swelling. Although he was never unconscious, some 4–5 hours later he developed repetitive jerking of the right face and arm. He was taken to his local casualty department where a diagnosis of serial focal motor seizures was made. His consciousness was then somewhat obtunded. A brain CT was performed which showed a small, discrete, spherical intracerebral haematoma in the left frontal lobe immediately beneath the skull at the point where he had been struck (similar in shape, but more hyperintense than the appearance in the figure B). The haematoma gave the distinct impression of a golf ball embedded in the surface of the cerebral hemisphere!

He was treated with parenteral anti-epileptic drugs and subsequently with thiopentone requiring ventilation for 48 hours while he was loaded with phenytoin.

He was maintained on phenytoin for 12 months but subsequently this was withdrawn and he has remained seizure free.

A 5 year old girl was struck on the forehead above the right eye by a golf ball struck 10 metres away. On arrival in the accident and emergency department she was fully alert, orientated, and neurologically intact. A laceration was present but there had been no apparent impairment of consciousness or vomiting. However, 90 minutes after the injury she had a generalised tonic clonic seizure lasting 25 minutes. She was intubated and ventilated. A CT scan showed a very small depressed fracture with minimal haemorrhagic contusion in the cortex of the right frontal lobe (figure C). She was woken and extubated later that day. She has had no further seizures

A 12 year old boy was practising golf with a friend. He was struck on the front of the head by a golf ball which rebounded a considerable distance after striking him. He did not lose consciousness and had no more than localised pain, tenderness, and bruising at the site of impact. He did not seek any medical advice about the injury. Over the next 4 years he had three well documented tonic-clonic seizures that started during sleep.

A CT scan 3 years after the original injury showed a small, wedge shaped area of low density affecting the cortex close to the point at which he recalls being struck (figure D).

The heads of these four young people were all subject to contact with golf balls which at club level travel at speeds of up to 130 miles/hour. Each had post-traumatic seizures, three early and one late, despite the apparent absence of post-traumatic amnesia.

Patients 1 and 2 would indicate that this kind of injury is capable of transferring energy across the skull, independent of a skull fracture, to cause an acute extradural or cortical haematoma.4 In patient 4 the lesion identified at a later date by CT is consistent with the late consequences of a localised intracranial haematoma. It therefore seems reasonable to assume that the late epilepsy in patient 4 was also related to the initial golf ball injury.

In the third patient, a minor depressed fracture and contusion were again associated with an early seizure without evidence of intervening impairment of consciousness.

It does therefore seem that golf ball injuries are capable of giving rise to both acute symptomatic seizures and late epilepsy without causing post-traumatic amnesia, skull fracture or dural tear. CT evidence, however, would predict the possibility of seizures in these examples in whom the development of post-traumatic epilepsy probably results from the physical properties of golf balls and their ability to transmit considerable mechanical energy at a small site of impact. The problem is one of which spectators on golf courses (and their doctors) should be aware.

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