The area just in front of the central sulcus, referred to as the pre-central gyrus (see Figure 5.1), is the origin of the motor fibres that innervate the muscles on the opposite side of the body. This pathway is referred to as the corticospinal tract and it crosses the midline at the level of the foramen magnum, the junction of the lower end of the brainstem and the upper end of the cervical spinal cord. Lesions affecting the pre-central gyrus will result in a contralateral hemiparesis affecting the face, arm and leg although, one limb may be weaker than the other and the face may be affected to a variable degree (partial weakness) or with hemiplegia (total weakness).

The clues that the hemiparesis is derived from a lesion in the frontal lobe are:

• conjugate eye deviation, in which the eyes look away from the side of the weakness and towards the side of the lesion due to involvement of the area of the frontal lobe that controls conjugate deviation of the eyes to the opposite side

• cortical sensory signs due to associated involvement of the parietal lobe on that side

• non-fluent dysphasia with dominant hemisphere lesions.

Very rarely, an irritative lesion can result in a contralateral hemiparesis with the eyes deviated to the side of the weakness and away from the side of the pathology, mimicking a pontine lesion in the brainstem where there is an area responsible for conjugate deviation of the eyes to the same side. When this area of the brainstem is affected the eyes deviate away from the side of the lesion and towards the side of the paralysis.

Changes to personality or behaviour

The pre-frontal region is that part of the frontal lobes anterior to the motor cortex and the motor speech area. Diseases affecting this region of the frontal lobe result in changes to personality or behaviour best summarised by the phrase ‘he/she is not him/herself’.

These patients can lose spontaneity and initiative and appear apathetic and depressed or, at the other end of the spectrum, patients can appear to ‘have a short fuse’. In this situation patients can become aggressive and violent, even after a trivial incident. This is seen following some head injuries. Patients with frontal lobe pathology can develop an elevated mood and behave inappropriately, such as the vicar’s wife who begins to tell dirty jokes and who was subsequently diagnosed with a meningioma (a benign tumour) in the frontal lobe.

If the olfactory tracts that lie beneath the frontal lobe are also affected, there can be an associated unilateral or bilateral anosmia (loss of the sense of smell).

An inability to perform acts voluntarily or to make decisions is seen in patients with pre-frontal problems and is termed abulia, reflecting pathology in the medial aspect of the frontal lobes. Abulia sometimes occurs with a subarachnoid haemorrhage (bleeding into the subarachnoid space) from vasospasm of the anterior cerebral artery related to a ruptured berry aneurysm on the anterior communicating artery (see Chapter 10, ‘Cerebrovascular disease’).

Difficulty walking

Another presentation of patients with frontal lobe pathology is apraxia of gait. The history is one of progressive difficulty walking in the absence of any weakness, sensory disturbance, ataxia or extrapyramidal dysfunction to account for the difficulty walking. It is as if the patient has forgotten how to walk. This is discussed in Chapter 12, ‘Back pain and common leg problems with or without difficulty walking’.

There are a number of frontal lobe signs, referred to as primitive reflexes, because they are present in normal babies and may or may not be seen in patients with frontal lobe pathology. These include:

• a grasp reflex, where the patient involuntarily grasps an object (usually the examiner’s hand) placed in the palm of their hand

• a positive palmo-mental reflex, where the palm of the hand is stroked and there is retraction of the ipsilateral chin beneath the lips

• a pout reflex, where the patient purses the lips when a stimulus is applied to them.

Although changes in personality and behaviour may be one of the presenting symptoms of dementia, severe depression can produce a similar clinical picture termed ‘pseudo-dementia’.

THE PARIETAL LOBES

Patients with parietal lobe problems may present in a number of ways:

• speech disturbance such as fluent dysphasia and, if Wernicke’s area in the posterior temporal lobe is also affected, the patient may also present with confusion (discussed in the section ‘Disturbances of speech’ below)

• disturbances of vision in the contralateral visual field

• lost and disoriented patients who appear to be lost or disorientated even in a familiar environment

• a concerned relative brings the patient for assessment, as some patients are not even aware of any problem at all and the problem is only detected when another person observes that there is something wrong.

Visual disturbances can occur in both dominant and non-dominant hemisphere problems; dysphasia is a feature of dominant hemisphere problems; being lost, disoriented and unaware that anything is amiss are very typical features of problems in the non-dominant hemisphere.

In both the dominant and non-dominant hemispheres, there are visual pathways that pass through and sensory pathways that terminate in the parietal lobe. If the so-called ‘primary pathway’ is affected, there will be a contralateral loss of function. If the ‘primary pathway’ is intact but the so-called ‘secondary association areas’ are affected, there will be a contralateral inattention with double simultaneous stimuli where the patient is not aware of the stimulus on one side when the other side is stimulated in the same manner simultaneously.

Speech disturbance (dysphasia) and the term RAAF (an abbreviation for the Royal Australian Air Force) best describe the features of problems in the dominant hemisphere, while the term ‘lost in space’ is the easy way to remember the characteristics of non-dominant parietal lobe problems (see Table 5.1). RAAF refers to the clinical findings seen in dominant parietal lobe problems and, in its pure form, is referred to as Gerstmann’s syndrome (for an explanation of RAAF, see ‘Gerstmann’s syndrome’ below).

TABLE 5.1

Summary of the clinical features with lesions of the dominant and non-dominant parietal lobes

^∗It can be seen that sensory and visual symptoms together with the unique parietal cortical signs are common to both the dominant and non-dominant parietal lobes. It is the speech disturbance and the parietal lobe abnormalities associated with Gerstmann’s syndrome in the dominant hemisphere and the characteristic abnormalities seen in the non-dominant hemisphere (referred to as ‘lost in space’) that differentiate between the two hemispheres.

^∗∗Either loss of vision in the opposite visual field (hemianopia) or loss of vision in the upper or lower aspect of the visual field on the opposite side (quadrantanopia).

Abnormalities of vision

• Contralateral loss of vision. The optic radiation from the contralateral visual field passes through the parietal lobes to the occipital lobe (see Figure 5.1). If the ‘primary pathways’ are affected, there will be a loss of vision on the contralateral side resulting in a lower quadrantanopia if only the parietal lobe is affected, but often the optic radiation fibres in the temporal lobe are also affected and the resulting deficit is a contralateral homonymous (the visual field disturbance is identical when each eye is tested separately) hemianopia.

• Contralateral visual inattention. If the ‘primary visual pathways’ are preserved, but the so-called ‘secondary association areas’ are affected, there will be visual inattention elicited with double simultaneous stimuli. The patient is unable to appreciate the visual stimulus in one visual field, usually a moving finger applied simultaneously to both visual fields, but can if only one visual field is stimulated at a time.