Patrick Haggard, Department of Psychology, UCL
Lecture 8. Some selected aspects of motor cortex damage in man
Introduction
The most common cause of MI damage in man is stroke (i.e., sudden failure of blood supply to the brain, for any one of a number of reasons). MI receives blood supply from the middle cerebral artery (MCA), which seems to be particularly vulnerable.
The most important consequence of stroke affecting MI in those who survive is hemiplegia-paralysis of muscles on the side of the body opposite the affected cortex. This demonstrates the crucial role of the corticospinal tract in human movement. Because the blood supply to adjacent areas is normally affected too, leading to loss of contralateral sensation (if SI is affected), and neglect of the left half of space (if the right parietal lobe is affected). Spasticity typically accompanies hemiplegia, due to failed cortical inhibition of spinal reflex circuits.
Hemiplegia gradually resolves, and movement returns to the affected muscles over a period of months. Primate studies (Lawrence and Kuypers, 1968) found that all movements, except for independent finger movements) returned after severing the corticospinal tract, and hypothesised that recovery was due to other motor pathways, primarily in the brain stem, taking over. The idea of substituting another motor area has recently been tested in man, by PET studies of finger movement in recovered stroke patients (Chollet et al., 1991). They found that the ipsilateral (intact) MI was abnormally activated when moving the fingers on the affected side. In man, the small ipsilateral (uncrossed) component of the corticospinal tract may be brought into play when the normal pathways are damaged. (These sort of "hemispheric substitution" would have been missed in bilateral lesion experiments like Lawrence and Kuypers). It is interesting to ask whether the ipsilateral projection does anything useful in normal function, or is it an evolutionary vestige of the days when we performed all actions bimanually?
Anosognosia
Anosognosia is "denial of illness". Cutting (1978) found that 58% of right hemisphere strokes denied their hemiplegia early after stroke, and refused to admit to any weakness in their left arm. This belief typically remains despite manifest demonstration that it is paralysed. Many other patients show bizarre attitudes to their paralysed limb (anosognosic phenomena), while not actually denying paralysis. The most common are dislike/hatred of the paralysed limb (misoplegia) and nonbelonging (belief that the arm does not belong to them, and is either someone else's arm). Anosognosia is generally fairly short-lived, often lasting only a few days immediately after stroke.
The pathology underlying anosognosia is very confusing. Most authors suggest you need a combination of hemiplegia with some other deficit due to additional brain damage caused by the stroke, e.g., sensory loss (Levine et al., 1991), inattention (Bisiach et al., 1991; Cutting, 1978; Hier et al., 1983), intellectual confusion (Levine et al., 1991). There is almost no agreement between studies. Revealingly, House and Hodges (1988) described a patient with hemiplegia and denial, but without any of the above deficits. It seems likely, though, that inability to attend to the left of space is normally required. The sites of brain damage, over and above that causing hemiplegia, is rather unclear: perhaps the temporoparietal junction, at least in many cases (Hier et al., 1983)?
Anosognosia for hemiplegia (AHP) is NOT an inevitable consequence of MI damage, but it is psychologically interesting, since it shows how important the ability to make voluntary movements is to a balanced sense of who we are: our personal identity. AHP shows that we are reluctant to accept absence of voluntary movement. Why? The psychological challenge is to explain why patients beliefs about their motor ability can drift so far from reality. Failure of attention may be part of the explanation for AHP: if you don't attend to your left arm you might not realise anything was wrong with it, and therefore assume it was normal, as if nothing had happened to it. You might not accept evidence that your left arm was paralysed if you could not process any information on the left side. However, this explanation does not account for phenomena like misoplegia (rather, it would imply that people never thought about their left arm at all), nor does it explain House and Hodges' patient.
A related phenomenon, which is equally challenging is somatoparaphrenia (delusional beliefs about the body). A few patients, who may or may not deny their hemiplegia, develop elaborate and very firm beliefs about their limbs. They may have too many, they may be distorted, inanimate, severed or in other ways bizarre (Halligan, Marshall and Wade, 1995). The limb quite often belongs to a specified other person (Bisiach et al., 1991).
Psychologically, AHP, anosognosic phenomena and somatoparaphrenia tell us about how important the ability to move is to our identity. There is a failure to update the "body schema" to reflect the paralysed limb. This seems to be due to a psychological unwillingness to accomodate the immobile limb within the body schema: the limb may be disliked or mistrusted, and patients will exile the limb from their body, seemingly to avoid having to accept the real deficit. Patients seem prepared to completely suppress "rationality" in order to defend their body schema in this way: they can develop an encapsulated psychosis which is very resistent to evidence. House and Hodges' patient could accept the weakness of her left limbs, but still claimed to be able to walk, drive a car etc. Is voluntary action so vital to our personal identity that we will go "mad" rather than forgo it?
References
Halligan PW, Marshall JC & Wade Dt (1995). Unilateral somatoparaphrenia after right hemisphere stroke: a case description. Cortex, 31, 173-182.
Cutting J (1978). Study of anosognosia. Journal of Neurology, Neurosurgery and Psychiatry, 41, 548-555.
Hier DB, Mondlock J & Caplan LR (1983). Behavioral abnormalities after right hemisphere strole. Neurology, 33, 337-344.
Levine DN, Calvanio R & Rinn WE (1991). The pathogenesis of anosognosia for hemiplegia. Neurology, 41, 1770-1781.
House A & Hodges J (1988). Persistent denial of handicap after infarction of the right basal ganglia: a case study. Journal of Neurology, Neurosurgery and Psychiatry, 51, 112-115.
Bisiach E, Rusconi ML & Vallar G (1991). Remission of somatoparaphrenic delusion through vestibular stimulation. Neuropsychologia, 10, 1029-1031.
Chollet F, DiPiero V, Wise RJS, Brooks DJ, Dolan RJ & Frackowiak RSJ (1991). The functional anatomy of motor recovery after stroke in humans: a study with positron emission tomography. Annals of Neurology, 29, 63-71.
Lawrence DG & Kuypers HGJM (1968) The functional organization of the motor system in the monkey: I. The effects of bilateral pyramidal lesions. Brain, 91, 1-14.