The collection and grouping of symptoms facilitate anatomical localisation of lesions within the central and peripheral nervous systems. Cerebration can be altered in psychiatric as well as organic disease and its various components, such as behaviour, attitude, emotion, thought process, intelligence and insight.

Of particular note in the neurological history are disturbances of consciousness (table 1), orientation in time and space, memory, speech, vision, and motor and sensory function. Headache is a common symptom, particularly in raised intracranial pressure, but it lacks specificity since it occurs in many other complaints. The Glasgow Coma Scale (table 2) provides a grading system of coma in relation to head injuries, that is used for the initial assessment and monitoring progress.

Note the frequency, timing, duration and progress of symptoms, and what the patient was doing at the time of onset of faints, falls or fits. Epileptic fits may be accompanied by tongue biting and urinary incontinence. Associated chest pain, palpitations or dyspnoea may indicate a cardiac or respiratory aetiology for these symptoms.

Speech disturbances are primarily due to abnormalities of articulation (dysarthria and anarthria) or of the organisation of language (dysphasia, aphasia). The muscles of the palate, tongue, larynx and pharynx have bilateral cortical innervation. Thus disturbances of articulation require damage to a lower motor neurone (cranial nerve), the nucleus (bulbar palsy) or bilateral upper motor neurone damage (pseudobulbar palsy). Basal ganglia disease produces slow and monotonous speech, whereas cerebellar disorders characteristically produce staccato or scanning speech.

Table 1 Coma

Drugs/ChemicalsAnesthetics Overdose Reaction (e.g. Reye’s syndrome) Addictive/recreational Alcohol Poisons (e.g. weedkiller, carbon monoxide)
Infection: Encephalitis, MeningitisPrion disease Viral: Hemorrhagic, nonhemorrhagic Bacterial: Brucellosis, meningococcal, syphilitic, tuberculous Protozoa and worms: Amebic, cysticercosis, malaria, dracunculiasis, toxoplasmosis, trichinosis, visceral larva migrans trypanosomiasis (sleeping sickness), schistosomiasis,
TraumaCerebral damage, hemorrhage, oedema
EndocrineHypo/hyperglycemia Hypo/hypercalcemia Myxedema Pituitary and adrenal disorders
MetabolicMetabolic acidosis. Hypo/hypernatremia
Organ failureHepatic, renal, respiratory
Benign and malignant, primary and secondary tumorsSpace occupying lesions
VascularInfarction Hypertensive encephalopathy Thrombosis Embolism Hemorrhage (intracerebral, brain stem, subarachnoid)
MiscellaneousPostepileptic seizure, hypothermia, hyperpyrexia, Wernick’s encephalopathy

Table 2 Glasgow coma score

RESPONSEDETAILS & SCORE
Best eye response (E)Eyes open spontaneously 4 - Eye opening to verbal command 3 - Eye opening to pain 2- No eye opening 1
Best verbal response (V)Orientated 5 - Confused 4 -Inappropriate words 3 - Incomprehensible sounds 2 -No verbal response 1
Best motor response (M)Obeys commands 6 - Localising pain 5 - Withdrawal from pain 4 - Flexion to pain 3 - Extension to pain 2 - No motor response 1
Coma Score = E + V + M (minimum = 3; maximum = 15) Coma Score of 13 or higher correlates with a mild brain injury, 9 to 12 is a moderate injury and 8 or less a severe brain injury: but the components should be presented with the score

Damage to Broca’s area (precentral cortex of the dominant hemisphere) produces an expressive dysphasia, the patient knowing what to say but unable to produce words. Mild degrees present as failure to name common objects and names (nominal aphasia). These conditions are commonly accompanied by inability to write (agraphia).

Dysphasia may also be produced by lesions of the parietal region due to failure of understanding of the spoken or written word (receptive aphasia, word deafness and word blindness). If Broca’s area is not affected the subject may produce a stream of disconnected words (jargon aphasia). More commonly, extensive lesions affect the expression as well as the understanding of speech (global aphasia).

Disturbances of memory may be short or long term; the former is frequently due to organic disease and may be reversible. Visual symptoms are considered with the cranial nerves (page 29).

Motor symptoms include paralysis, spasticity, incoordination and abnormal movements. Mild paresis may present with fatigue and weakness, such as diminution of grip, dropping things and toe catching when walking. Spasticity may be due to pyramidal or extrapyramidal disease. In milder forms it presents with stiffness.

Cerebellar dysfunction interferes with everyday activities, such as writing and eating, or may produce a mild intension tremor and loss of balance. Abnormal movements include the tremor of Parkinson’s disease, tics and choreiform movements.

The distribution of the sensory disturbances of anesthesia, parasthesia (pins and needles), numbness, increased sensation (hyperesthesia) and pain, provide important information on the localisation of lesions; visceral pain may be referred to somatic dermatomes.