Case study - An unexpected development following a minor head injury

Minor head injury may trigger an acute polyneuropathy, says Dr Michael Barrie.

Cerebrospinal fluid tests for oligoclonal bands were negative (Photograph: SPL)
Cerebrospinal fluid tests for oligoclonal bands were negative (Photograph: SPL)

Lisa, a healthy 40-year-old patient, came to see me following a head injury.

The injury was not severe: she was not knocked out and there was no apparent wound to the scalp. By the next day, however, she had developed paraesthesia in her feet, a stiff neck and pain across her upper back.

Careful examination showed paraspinal spasm in her neck muscles; there was also tenderness and spasm in both the sternocleidomastoid and trapezius. Lisa was alert, fully orientated and showed no focal neurological signs.

I reassured her that she was experiencing muscular pains following the head injury - due to the impact the knock must have had on the soft tissues of the neck. However, the following day, Lisa's husband called to say she was no better and was now feeling weak and lethargic. Although the head injury itself did not sound significant, I was confident her symptoms had arisen following the injury.

Further investigations
I decided to arrange an urgent MRI scan of her brain. I also sent off some baseline blood tests to check parameters, such as vitamin B12 and thyroid status, FBC and so on. Doubt was creeping into my mind - was the head injury a confounding element of the story? Had it unmasked some other pathology?

Re-examining the patient
The brain scan and blood results were all normal. I arranged to see Lisa to explain this and also to re-examine her.

As she approached the surgery she was leaning heavily on her husband for support, being almost totally unable to walk unaided. She was unsteady and very weak; even at rest she could not stand unsupported.

Her gait was wide-based and shuffling. Lisa had evidence of proximal weakness in her lower limbs and I could not elicit knee jerk reflexes. She had pins and needles and numbness in both hands, both feet and in her buttocks and groin.

The differential diagnosis was an acute cauda equina lesion or an acute inflammatory demyelinating polyneuropathy, such as Guillain-Barre syndrome.

Lisa did not have any disturbance of sphincter function nor the classic 'saddle anaesthesia'. Although the numbness in the buttocks was worrying, the presence of paraesthesia and hypoaesthesia in the upper limbs did not fit cauda equina.

I referred Lisa urgently to a consultant. He found she had neither knee nor ankle reflexes. Urgent MRI of cervical and lumbosacral spine was normal. Lumbar puncture was performed and the cerebrospinal fluid tested for cytology and oligoclonal bands. Both were negative. Nerve conduction studies and electromyography were consistent with acute Guillain-Barre syndrome.

Lisa was commenced on IV IgG and this was continued for five days. She was up and about within a few days, and when I saw her three weeks later she had made a full recovery.

An acute polyneuropathy
Guillain-Barre syndrome is an acute, inflammatory polyneuropathy. A prodromal malaise with nausea, headache and limb pains is rapidly surmounted by a progressive and ascending paralysis. Weakness in the legs may spread to the upper limbs and the face along with complete loss of deep tendon reflexes. This can lead to respiratory dysfunction and, as such, the acute presentation can be a neurological emergency.

With prompt treatment by IV immunoglobulins and supportive care, most patients will regain full functional capacity. However, death may occur if severe pulmonary complications and autonomic nervous system problems are present.

This syndrome often follows an acute infectious process and Campylobacter jejuni has been suggested as a likely cause.

Around 60% of cases of Guillain-Barre syndrome do not have a known cause; of topical interest is the possible association between H1N1 vaccination and acute Guillain-Barre syndrome. A literature search found documented cases of Guillain-Barre following head injury.1

There is no doubt that in Lisa's case, the onset of neurological symptoms following her head injury prompted me to consider an intracerebral bleed; the normal MRI that followed was falsely reassuring. Doctors need to be alert to the relevance of similar incidents which may herald the onset of an acute, inflammatory polyneuropathy, such as Guillain-Barre syndrome.

  • Dr Barrie is a GP in Kingston-upon-Thames, Surrey

Reference
1. Duncan R, Kennedy PG. Guillain-Barre syndrome following acute head trauma. Postgrad Med J 1987; 63(740): 479-80.

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