Dysarthria is disordered articulation – production and/or coordination of speech. Anarthria is complete inability to articulate.
Dysphonia is disordered voice production, caused by passage of expired air over poorly vibrating or paralysed vocal cords. Aphonia is complete inability, or apparent inability to produce sounds.
Temporal Lobes
Many small (<2 cm) unilateral temporal lesions are silent. Epilepsy is common (Chapter 8). Upper quadrantic hemianopia is seen when the forward‐looping fibres (Meyer’s loop) are damaged. A lesion in the posterior dominant anterior temporal lobe can cause a posterior (Wernicke) aphasia (Chapter 5), or much less commonly, and usually when bilateral, word deafness, that is inability to understand speech, caused by damage to auditory areas in or near Heschl’s gyrus.
Non‐dominant anterior temporal lobe lesions are sometimes associated with inability to recognise faces (prosopagnosia). Unilateral mesial temporal lobe lesions can also produce subtle changes in memory, more marked for verbal material in the dominant, and faces and topographical features in the non‐dominant hemisphere.
Bilateral temporal lobe lesions, such as post‐herpes simplex encephalitis can cause profound memory loss for recent events. Bilateral damage in primates can cause hypersexuality, hyperphagia, and aggression (Klüver–Bucy syndrome). Sometimes, elements of this occur in Man, such as temper dyscontrol, but the usual outcome is amnesia and aimlessness.
Frontal Lobes
Many lesions remain silent. Frontal regions have connections with the basal ganglia and limbic systems, networks that mediate emotional, social and motivational behaviours. Lesions involving the dorsal frontal convexities can cause impassivity and apathy – more medial lesions may even cause mutism, while orbito‐frontal lesions are more likely to produce disinhibition. However, localisation is distinctly imprecise.
Lesions involving dominant inferior frontal gyrus cause anterior (Broca’s) aphasia.
Substantial damage such as traumatic frontal brain injury, direct or contra‐coup can cause disabling problems:
Abandonment of social inhibitions – from inopportune comments to more profound, such as urination, exposure or masturbation
Inappropriate jollity (witzelsucht) – tales overlong, unwanted, with loss of empathy
Apathy (abulia), lack of initiative, poor planning (dysexecutive problems)
Irritability, anger or the converse – placidity in the face of irritation
Distractability, or the converse – obsessions
Continuing one action when another is appropriate, a.k.a. motor perseveration
Utilisation behaviour: the patient sees a stethoscope and begins to use it.
Release of primitive programmes from early infancy, such as grasp, rooting or sucking reflexes can emerge. Bilateral frontal lesions, such as small vessel disease can lead to gait apraxia and failure to initiate walking (gait ignition failure), with urinary incontinence.
Alleged brain damage with behavioural change has become a common plea in claims following minor head injury. The patient and relatives are asked leading questions about features such as impulsivity, temper, fiscal ability, multi‐tasking, planning, depression and anxiety – all common problems in any event. There is no evidence that these are caused by brain injury following a minor blow to the head, with normal imaging. Frontal lobe seizures are described in Chapter 8.
Occipital Lobes
Field defects are mentioned in Chapter 14. Neglect or even denial of virtually complete visual loss (cortical blindness or Anton’s syndrome) are sometimes seen following bilateral infarction. An explanation for ‘blind sight’ (perception of objects when the occipital cortex is destroyed) is preservation of anterior visual pathways via the lateral geniculate bodies that are below the level of awareness. Epilepsy, with episodes of flashing lights or, rarely, more formed features, can occur with occipital lobe lesions.
Parietal Lobes
These integrate visual and somatosensory information, such as awareness of body parts and their relation to objects. A complex nomenclature has evolved. Attempts to associate precise areas to particular functions are bedevilled by variation between individuals, and because the cortex is not divided into discrete compartments. The following are seen with lesions of either parietal lobe:
Attention defects in the contralateral visual field and neglect of the opposite side
Lower quadrantic homonymous field defects
Astereognosis – inability to recognise common objects placed in the palm despite normal sensation
Agraphaesthesia – inability to recognise numbers drawn on the palm
Pseudo‐athetosis (waving about) and/or drift of an outstretched contralateral hand
Contralateral cortical sensory loss – impaired two point discrimination despite intact peripheral sensation.
Sensory epilepsy is sometimes a feature.
Dominant Parietal
Inability to execute a skilled movement despite no discernable weakness may be seen – apraxia. The patient may not respond to suggestions ‘imitate combing your hair’ or ‘pretend to turn a key’: a.k.a. ‘ideational’ apraxia. Alternatively, the patient may have difficulty imitating a meaningless gesture made by the examiner: ‘ideomotor’ apraxia. Typically, they are bewildered, moving the hand in a non‐purposive way or attempting to grasp the examiner’s hand.
Lesions may produce impairment of literacy skills: alexia, agraphia and acalculia. The rare constellation of these with finger agnosia (inability to name individual fingers and right–left disorientation) is known as Gerstmann’s syndrome. Auditory short‐term verbal memory can be impaired. Neglect of contralateral limbs is typically less prominent with a dominant than non‐dominant parietal lesion.
Non‐dominant Parietal
Patterns include:
Neglect of opposite limbs. Neglect can extend to denial that limbs belong to the patient.
Inability to draw shapes such as a house or a clock face. The left side of a picture drawn (such as numbers 1–5 on a clock face) tend to be omitted with a right parietal lesion, a.k.a. constructional apraxia.
Visual apperceptive agnosia – inability to perceive objects under poor viewing conditions or from an unusual angle.
Motor Abnormalities: Brain and Spinal Cord
Hemiparesis, hemiplegia, paraparesis, cerebellar syndromes and disorders of movement are summarised here.
Hemiparesis
This is the weakness on one side usually from a pyramidal tract lesion. Hemiplegia means total paralysis. See Examination (above). Hemiparesis without other UMN signs