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J R Soc Med 2003;96:23-27
doi:10.1258/jrsm.96.1.23
© 2003 Royal Society of Medicine

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J R Soc Med 2003;96:23-27
© 2003 The Royal Society of Medicine

Babington's aphasia—overcoming left hemisphere trauma

E H Jellinek DM FRCP  

7 Oxgangs Road, Edinburgh EH10 7BG, Scotland, UK

Anthony Babington was 24 and a company commander in the 1st Dorset Regiment when he was wounded by shrapnel in Holland early in the morning of 2 November 1944, in the aftermath of the Arnhem campaign. His story is in his own writings1,2 and in his army medical records3, both quite exceptional in detail and perception.

CASE HISTORY

He was felled by the shell burst and briefly unconscious, and had sustained a left parietal penetrating injury which made him mute and hemiplegic. He was evacuated by stretcher, ambulance and plane. ‘During the flight I felt something stiff and cold on the right side of my chest. I puzzled about it for a while before it dawned on me that it was my right arm, heavy, insensate and quite paralysed... At one point I thought the end had come...’2. On the evening of the same day he reached the Military Hospital for Head Injuries at St Hugh's College, Oxford.

X-rays showed ‘a large MFB [metal foreign body] deep in the left parietal lobe just above the ventricular roof but may impinge on it.’ On 3 November Major C A Calvert4 operated on a semiconscious, globally aphasic man who had a right hemiplegia, hemianaesthesia, and hemianopia (Figure 1):



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Figure 1. C A Calvert's operation diagram of 3 November with measurements of site of lesions from X-rays

 
‘... wound stank horribly... contamination with hairs and dura down brain track—marked oedema... toothpaste brain and clot... bone chips indrawn about 2 cm, metallic body about 4 cm from cortex, inner end about 6 cm... debrided... many toothpaste pockets extending laterally from track... area of cortex destruction about 4 cm x 4 cm... gush of CSF... ventricle into which MFB had protruded... 5000 U penicillin... dura left open... drain...’3.

After the operation Anthony Babington recalled1,2 gesticulating with his left hand to indicate that he needed treatment for head pain, something to drink, or a urine bottle. When asked to write his home address with his left hand ‘I knew exactly what I intended to write but I was dismayed to find myself drawing a series of short and very crooked lines... when shown a newspaper I could see letters but not understand them... might have been Chinese.

‘I woke one morning feeling slightly better. The night sister said "You are over the worst and out of danger... The doctors think you might get back a little movement in your right side, in the leg at any rate. But I am afraid they think it unlikely that you will ever be able to speak again".’

This forecast also ended a close personal relationship.2

Like Dr Johnson after his stroke5, he was comforted by his ability to say the Lord's Prayer silently.

In the medical records3 Captain G Northcroft wrote on the fourth postoperative day that there was now no hemianopia and that he could indicate yes and no by head movements. On 11 November he could just utter ‘well’, and on the 14th there were a few single words, and ‘speech therapy’ was started by a sympathetic lady who had trained as a singing teacher and by a Norwegian fellow patient1,2.

Early progress
He began to try to read a book: ‘... laborious... words slowly... wrong lines... Writing even more discouraging... left hand awkward... entirely lost the art of spelling... even ridiculously simple words. I did not seem capable of visualising them on paper’1. Three months later his speaking, reading and left-handed writing had improved enough to make feasible his intention to take up law studies, according to psychometric testing by Major W R Reynell3. He was discharged from hospital in May 1945, with the advice to take up market gardening. But he went to the Middle Temple later in 1945, and in 1948 he qualified as a barrister, having had the use of an amanuensis for his written examinations1.

The next 57 years
Ever since, his speech has continued to be slow, with a slight stammer, and persistent inability to utter some words which he has managed to cover by circumlocution; there are no wrong words. His reading also has remained slow, both silent reading and reading aloud, but adequate for public performance. He achieves a slow sinistral script which looks like his old dextral writing but with persistent mis-spelling, even of common words (Figure 2). He has been rendered moderately dyscalculic by the injury, but considers his powers of reasoning, and his memory for abstract data, for places and faces, as good as before. He never experienced difficulty in understanding spoken speech. He had a successful career as a barrister, at first in chambers, then for 8 years as metropolitan magistrate, and lastly as circuit judge until beyond the usual retiring age2.



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Figure 2. Dysgraphia in 1946 and 1994: spelling problems and elisions

 

He has also written ten books, three of which were republished. Two are autobiographical1,2, the others are on legal and military history. His writings were influential in changing the public attitude to the execution of soldiers in the First World War for desertion and for cowardice, and to ‘shell shock’.

He had bad headaches in the first post-traumatic year, and intermittently later, related to low-grade skull infections until the tantalum skull implant was removed by Mr C Connolly in 1975. In the early years he had a few partial (right hemisensory) seizures, treated with phenobarbitone; he stopped taking this because of retardation, and the attacks have remained in abeyance. The right hemisensory loss has persisted, as has near-total paralysis of the right upper limb. The initial right lower limb paralysis improved sufficiently to allow pleasurable walking of up to five miles, but has worsened in his 70s, and he is now limited to a slow few hundred yards with a walking-stick. He also weathered long spells of inpatient treatment, with a lobectomy in 1951, for pulmonary tuberculosis, and later acute surgery for a duodenal ulcer, and aortic valve surgery. Despite his disabilities he retains his joie de vivre at the age of 82.

COMMENT

Site of lesion and clinical features
Speedy and expert neurosurgery, as well as the newly available penicillin, were lifesaving. But he was left with a deficit of parietal cortex (‘4 cm across’) extending deeply through the white matter down to the lateral ventricle. There must also have been damage to the left (frontal) motor cortex, or to its connections, to cause the right hemiplegia.

The initial aphasia was termed ‘global’3, but he did not seem to lose understanding, even at his worst. Much of this, like the transient right hemianopia, must have been due to cerebral oedema. The penetrating shrapnel and bone chips impinged just in front of, and above, the temporal gyri described in 1874 by Wernicke6 as the site of sensory (i.e. receptive) aphasia, and a little further from Broca's more anterior low frontal site of motor or expressive aphasia (Figure 3). Both Broca and Wernicke made their discoveries from cases of cerebrovascular disease; Broca in particular was severely criticized in 1906 by Pierre Marie7 for anatomical oversimplification, as Broca's extant post-mortem specimen had shown more extensive lesions than just in the left second and third frontal convolutions.



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Figure 3. Centre of lesion in supramarginal gyrus at intersection of lines from diagram (see Figure 1).

C=Central sulcus; B=Broca's area; W=Wernicke's area: superimposed on sagittal MRI scan of normal brain

 

Accordingly aphasiologists preferred the ‘crisper’ trauma material from the wars of the last two centuries—Larrey8 from the Napoleonic wars, Henry Head9, Pierre Marie10 and Kurt Goldstein11 from the First World War, and A R Luria12 and Ritchie Russell13 from the Second World War. The studies of the last dealt with the 1100 head injuries treated at St Hugh's College, Oxford3 and the other British neurosurgical units.

While confirming the great importance of Broca's frontal and Wernicke's temporoparietal speech areas, both the Russian12 and the British13 compositions agreed on a wider left hemisphere distribution of lesions causing aphasia, but clustering around Broca's and Wernicke's areas, with, conversely, an absence of aphasia after more distant left hemisphere lesions (Figure 4). Right hemisphere lesions were exceptional in causing aphasia, even in left-handers. Freda Newcombe14 conducted a more intensive late assessment in 153 selected patients from the above 1100 military head injuries, noting in particular professional achievers. Anthony Babington is not discernible in her14 or in Russell's13 accounts.



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Figure 4. Composite diagrams of penetrating left hemisphere lesions causing aphasia (x), and not causing aphasia (o) (from Ref 13)

 

Recovery
Apart from the spontaneous resolution of brain oedema after C A Calvert's operation, leading to the improvement recorded in the first few weeks, his later recovery may be attributed in part to his determination and vocation. There is also the theoretical concept, in a young man, of reserve brain potential and ‘plasticity’15, linked perhaps to the degree of left hemisphere dominance and right hemisphere speech functions16.

The notion of left hemisphere dominance goes back to the observations of Dax and Broca in the 19th century, and has an anatomical basis in specially developed areas of cortex on the left side17. While most left-handers, like right-handers, have their speech ‘centres’ on the left side of the brain, as judged by Wada's intracarotid sodium amytal injection testing18, they may still recover better than right-handers after left hemisphere lesions with aphasia12,19. One needs to consider degrees of left-handedness or of ambidexterity, and any family history of left-handedness, or left eye or ear dominance16. While dextrad for everything else, Anthony Babington was a left-handed bowler at cricket and a left-footed footballer as a boy.

Beside the overall better outlook in traumatic than in stroke aphasia20, Babington's high initial intelligence was probably also a good prognostic factor21, as opposed to the adverse prognostic factors of the immediate severity and ‘globality’ of the aphasia10 and of the concomitant hemiplegia.

Did the so-called speech therapy help his recovery? While there has been continuing interest in communication skills after severe brain traumas22, there has been no critical study of the value of speech therapy in aphasia23. The bulk of aphasia cases in peace-time are due to strokes, with inevitably great variability and a worse prognosis than in the mostly younger sufferers of traumatic aphasia—and, indeed, amateurs may do as well as trained speech therapists in stroke aphasia24.

Modern investigations such as positron emission tomography (PET) scanning25 and functional magnetic resonance imaging (fMRI)26 which can demonstrate changes in regional cerebral blood flow during various language tasks have greatly advanced our ideas of the anatomy and physiology of speech, beyond what had been derived from the deficits resulting from brain lesions: it has unfortunately not been possible to study Anthony Babington's communication skills in this way.

That he achieved so much in his two vocations as a lawyer and as a writer may serve as a warning to dismal prognosticians, and as a tribute to his personality.

Acknowledgments

I am most grateful to His Honour Anthony Babington for permission to write about him, and for his help; also to the late Dr Freda Newcombe for giving me access to the medical records at Oxford. I am obliged to David Jellinek and Charles Romanowski, of the neurosciences department, Sheffield, for demonstrating the neuroanatomy of the lesion by MRI superimposition.

REFERENCES

  1. Babington A. No Memorial. London: Heinemann, 1954

  2. Babington A. An Uncertain Voyage. Chichester: Barry Rose Law Publications, 2000

  3. Military Hospital for Head Injuries, Oxford: records(RAMC, Ministry of Pensions, Medical Research Council). St Hugh's College, Oxford

  4. Anon. Obituary: CA Calvert. BMJ1956; i:863 -5

  5. Critchley M. Dr Johnson's aphasia. Med Hist1962; 6:27 -44[Medline]

  6. Wernicke C. Der aphasische Symptomenkomplex. Breslau: Cohn & Weigert,1874

  7. Marie P. La troisième convolution frontale gauche ne joue aucune rôle spéciale dans la fonction de la langage. Sem Méd (Paris)1906; 26:241 -7, 493-500, 565-71

  8. Jellinek EH. An unlikely aphasiologist: DJ Larrey. J R Soc Med 2002;95:368 -70[Free Full Text]

  9. Head H. Aphasia and Kindred Disorders of Speech. Cambridge: Cambridge University Press,1926

  10. Marie P, Foix C. Les aphasies de guerre. Rev Neurol 1917;31:53 -87

  11. Goldstein K. After-effects of Brain Injury in War. New York: Grune & Stratton,1948

  12. Luria AB. Traumatic Aphasia—its Syndromes, Psychology and Treatment. The Hague: Mouton,1970

  13. Russell WR, Espir MLE. Traumatic Aphasia... in War Wounds of the Brain. London: Oxford University Press,1961

  14. Newcombe F. Missile Wounds of the Brain: a Study of Psychological Defects. London: Oxford University Press,1969

  15. Geschwind N. Late changes in the nervous system. In: Stein D, Rosen J, Butters N, (eds) Plasticity and Recovery of Function in the CNS. New York: Academic Press, 1974

  16. Zangwill O. Cerebral dominance and its relation to psychological function. In: Reuck A, O'Connor M, eds. Disorders of Language. London: Churchill, 1964

  17. Galaburda A. Anatomical asymmetries. In: Geschwind N, Galaburda A, eds. Cerebral Dominance. Cambridge, Mass: Harvard University Press

  18. Rasmussen T, Milner B. Lateralisation of speech function. Ann NY Acad Sci1977; 299:355 -69

  19. Hecaen H, Ajuriaguerra J. Left-handedness and Cerebral Dominance. New York: Grune & Stratton,1964

  20. Kertesz A, McCabe P. Recovery patterns and prognosis in aphasia. Brain1977; 100:1 -18[Free Full Text]

  21. Newcombe F. Very late outcome after focal war-time brain wounds. J Clin Exp Neuropsychol1966; 18:1 -23

  22. Snow P, Douglas J, Ponsford J. Conversational abilities following severe traumatic brain injury. Brain Inj1988; 12:911 -35

  23. Sellars C, Hughes T, Langhorne P. Speech and language therapy for dysarthria due to non-progressive brain damage: Cochrane review. The Cochrane Library Issue 2. Oxford: Update Software,2002

  24. David R, Enderby P, Bainton D. Treatment of acquired aphasia: speech therapists and volunteers compared. J Neurol Neurosurg Psychiatry 1982;45:957 -61[Abstract/Free Full Text]

  25. Weiller C, Isengee C, Rijntjes M, et al. Recovery from Wernicke's aphasia; a positron emission tomography study. Ann Neurol 1995;37:723 -32[Medline]

  26. Billingsley R, McAndrew M, Crawlwy A, et al. fMRI of phonological and semantic processing in temporal lobe epilepsy. Brain2001; 124:1218 -27[Abstract/Free Full Text]


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