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 is highly unusual in organic weakness.
Cerebellar Syndromes
Features of cerebellar disease are well defined. With a lateral cerebellar lobe lesion, there is rebound and dysmetria in the ipsilateral limbs, dysarthria and nystagmus. With a vermis lesion, there is ataxia of stance, trunk & gait, sometimes with negative Romberg.
There are two practical points:
First, if an expanding cerebellar mass lesion is suspected or found on imaging, there must be speedy liaison with a neurosurgeon. While all brain mass lesions are potentially serious, many tumours above the tentorium can be dealt with in an expectant manner. With a cerebellar mass progression can take place over hours or less. Secondly, to misdiagnose as non‐organic the ataxia of stance and gait of a midline lesion does happen. See cerebellar syndromes: (Chapter 17).
Movement Disorders
These can be divided into akinetic‐rigid syndromes, where poverty of movement predominates, and dyskinesias in which excessive movement is the principal feature. Akinetic‐rigid syndromes include idiopathic Parkinson’s, Parkinson‐plus, drug‐induced & post‐encephalitic parkinsonism, manganism (v.rare), childhood akinetic‐rigid syndromes and Wilson’s disease.
Dyskinesias include tremors, chorea, hemiballismus, myoclonus, tics, dystonias, paroxysmal and drug‐induced dyskinesias. The distinction between the two groups is artificial. For example, Parkinson’s can be primarily tremulous; Wilson’s disease can have features of akinesia with an unusual tremor.
No amount of writing surpasses seeing a movement disorder, either in the flesh or on video. See: Chapter 7.
Diagnostic difficulties occur. First, when akinetic‐rigidity becomes apparent, early idiopathic Parkinson’s disease tends to be over‐diagnosed. The reality, evident some years later, is another akinetic‐rigid syndrome. Parkinson’s is almost always asymmetrical, and also should be diagnosed with caution if rest tremor is not apparent. Progressive supranuclear palsy (PSP) or multiple system atrophy (MSA) tend to be symmetrical from the onset. Consider Wilson’s disease in akinetic‐rigidity, or dyskinesia below 40.
Benign essential tremor (BET), though common, can cause difficulty. Usually, tremor occurs when the limbs adopt a particular posture. However, forms of BET mimic benign tremulous Parkinson’s disease, and even cerebellar action tremor.
Early chorea is easy to miss – mistaken for fidgeting. Minor dystonia can also escape recognition. Non‐organic movement disorders are difficult; many labelled initially as functional have organic disease.
Paraparesis
Spastic paraparesis, meaning lower limb weakness of cord or, rarely, cortical origin, is a pivotal diagnosis. Prior to MRI, clinical examination had a major role in differentiating between cord compression and other causes of paraparesis.
The clinical picture begins with subtle features:
Scuffing the toes of shoes, often worse on one side
Stiffening of gait (spastic gait) with retention of a narrow base
Noticeable beats of ankle clonus (e.g. on a step or kerbstone)
Changes in lower limb sensation.
Spinal pain is common in cord compression. With a thoracic meningioma, pain at tumour level develops with an emerging spastic paraparesis and a sensory level, rising from below. The patient complains of numbness or altered sensation commencing in the feet, that marches upwards, over days, weeks or longer. Brown‐Séquard features (pyramidal signs on one side, spinothalamic on the other) may appear.
These features apply equally to tetraparesis (syn. quadriparesis).
The five principal features of a pyramidal lesion may not all be present. Pain may not be present in cord compression. Marked asymmetry can sometimes cause difficulty.
Two questions arise when signs of spastic paraparesis are found:
Is the paraparesis caused by cord compression?
Is the paraparesis the result of a condition in which it is part of the picture? Examples are:MSMNDSubacute combined degeneration of the cordSyringomyeliaCortical lesions such as a parasagittal meningioma, hydrocephalus and other brain lesions can occasionally cause paraparesis.
Paraparesis is also caused by many rarities, such as vascular anomalies of the cord, adrenoleucodystrophy and copper deficiency (see Chapter 16). There can be difficulties with the initial diagnosis: within primary care, especially when restricted to a brief telephone call, emergence of difficulty in difficulty in walking is not taken seriously, and early features of a paraparesis can pass unrecognised.
Brainstem Syndromes
