TRIPASS XR تري باس

 

Speech

Dysarthria refers to slurred or ‘strangulated’ speech caused by

articulation problems due to a motor deficit.

Dysphonia describes loss of volume caused by laryngeal

disorders.

Examination sequence

• Listen to the patient’s spontaneous speech, noting

volume, rhythm and clarity.

• Ask the patient to repeat phrases such as ‘yellow lorry’ to

test lingual (tongue) sounds and ‘baby hippopotamus’ for

labial (lip) sounds, then a tongue twister such as ‘The Leith

police dismisseth us.’

• Ask the patient to count to 30 to assess fatigue.

• Ask the patient to cough and to say ‘Ah’; observe the soft

palate rising bilaterally.

Disturbed articulation (dysarthria) may result from localised

lesions of the tongue, lips or mouth, ill-fitting dentures or

neurological dysfunction. This may be due to pathology anywhere

in the upper and lower motor neurones, cerebellum, extrapyramidal

system, or nerve, muscle or neuromuscular junction.

Bilateral upper motor neurone lesions of the corticobulbar tracts

cause a pseudobulbar dysarthria, characterised by a slow, harsh,

strangulated speech with difficulty pronouncing consonants, and

may be accompanied by a brisk jaw jerk and emotional lability.

The tongue is contracted and stiff.

Bulbar palsy (see Box 7.5 later) results from bilateral lower motor

neurone lesions affecting the same group of cranial nerves (IX, X,

XI, XII). The nature of the speech disturbance is determined by the

specific nerves and muscles involved. Weakness of the tongue

results in difficulty with lingual sounds, while palatal weakness

gives a nasal quality to the speech.

Cerebellar dysarthria may be slow and slurred, similar to alcohol

intoxication. Myasthenia gravis causes fatiguing speech, becoming

increasing nasal, and may disappear altogether. Parkinsonism may

cause dysarthria and dysphonia, with a low-volume, monotonous

voice, words running into each other (festination of speech), and

marked stuttering/hesitation.

Fig. 7.3 Testing for meningeal irritation: Kernig’s sign.

126 • The nervous system

cortical function can be difficult and time-consuming but is essential

in patients with cognitive symptoms. There are various tools, all

primarily developed as screening and assessment tools for dementia.

For the bedside the Mini-Mental State Examination (MMSE) and

Montreal Cognitive Assessment (MoCA) are quick to administer,

while the Addenbrooke’s Cognitive Examination is more detailed

but takes longer. None of these bedside tests is a substitute for

detailed neuropsychological assessment. The assessment of

cognitive function is covered in more detail on page 323.

Cortical function

Thinking, emotions, language, behaviour, planning and initiation of

movements, and perception of sensory information are functions of

the cerebral cortex and are central to awareness of, and interaction

with, the environment. Certain cortical areas are associated with

specific functions, so particular patterns of dysfunction can help

localise the site of pathology (Fig. 7.4A). Assessment of higher

2 Parietal lobe

Dominant side

FUNCTION

Calculation

Language

Planned movement

Appreciation of size,

shape, weight

and texture

LESIONS

Dyscalculia

Dysphasia

Dyslexia

Apraxia

Agnosia

Homonymous hemianopia

Non-dominant side

FUNCTION

Spatial orientation

Constructional skills

LESIONS

Neglect of non-dominant side

Spatial disorientation

Constructional apraxia

Dressing apraxia

Homonymous hemianopia

4 Temporal lobe

Dominant side

FUNCTION

Auditory perception

Speech, language

Verbal memory

Smell

LESIONS

Dysphasia

Dyslexia

Poor memory

Complex hallucinations

(smell, sound, vision)

Homonymous hemianopia

Non-dominant side

FUNCTION

Auditory perception

Music, tone sequences

Non-verbal memory

(faces, shapes, music)

Smell

LESIONS

Poor non-verbal memory

Loss of musical skills

Complex hallucinations

Homonymous hemianopia

1 Frontal lobe

FUNCTION

Personality

Emotional response

Social behaviour

3 Occipital lobe