TRIPASS XR تري باس

 

Dizziness and vertigo

Patients use ‘dizziness’ to describe many sensations. Recurrent

‘dizzy spells’ affect approximately 30% of those over 65 years

and can be due to postural hypotension, cerebrovascular disease,

cardiac arrhythmia or hyperventilation induced by anxiety and

panic. Vertigo (the illusion of movement) specifically indicates a

problem in the vestibular apparatus (peripheral) or, much less

commonly, the brain (central) (see Box 9.3 and p. 174). TIAs

do not cause isolated vertigo. Identifying a specific cause of

dizziness is often challenging but may be rewarding in some

cases, including benign paroxysmal positional vertigo (BPPV),

which is eminently treatable. As a guide, recurrent episodes of

vertigo lasting a few seconds are most likely to be due to BPPV;

vertigo lasting minutes or hours may be caused by Ménière’s

disease (with associated symptoms including hearing loss, tinnitus,

nausea and vomiting) or migrainous vertigo (with or without

headache).

Functional neurological symptoms

Many neurological symptoms are not due to disease. These

symptoms are often called ‘functional’ but other (less useful

and more pejorative) terms include psychogenic, hysterical,

somatisation or conversion disorders. Presentations include

blindness, tremor, weakness and collapsing attacks, and patients

will often describe numerous other symptoms, with fatigue,

lethargy, pain, anxiety and other mood disorders commonly

associated. Diagnosing functional symptoms requires experience

and patience (p. 363). Clues include symptoms not compatible

with disease (such as retained awareness of convulsing during

non-epileptic attacks, or being able to walk normally backwards

but not forwards), considerable variability in symptoms (such

as intermittent recovery of a hemiparesis), multiple symptoms

(often with numerous previous assessments by other specialties,

particularly gynaecology, gastroenterology, ear, nose and throat

and cardiorespiratory) and multiple unremarkable investigations,

leading to numerous different diagnoses. The size of a patient’s

case notes can sometimes be a clue in itself! Beware of labelling

symptoms as functional simply because they appear odd or

inexplicable. Like disease, most functional neurological disorders

follow recognisable patterns, so be cautious when the pattern

is atypical.

Past medical history

Symptoms that the patient has forgotten about or overlooked may

be important; for example, a history of previous visual loss (optic

neuritis) in someone presenting with numbness suggests multiple

sclerosis. Birth history and development may be significant, as

in epilepsy. Contact parents or family doctors to obtain such

information. If considering a vascular cause of neurological

symptoms, ask about important risk factors, such as other

vascular disease, hypertension, family history and smoking.

Stroke and transient ischaemic attack

A stroke is a focal neurological deficit of rapid onset that is

due to a vascular cause. A transient ischaemic attack (TIA) is

the same but symptoms resolve within 24 hours. TIAs are an

important risk factor for impending stroke and demand urgent

assessment and treatment. Hemiplegia following middle cerebral

artery occlusion is a typical example but symptoms are dictated by

the vascular territory involved. Much of the cerebral hemispheres

are supplied by the anterior circulation (the anterior and middle

cerebral arteries are derived from the internal carotid artery), while

the occipital lobes and brainstem are supplied by the posterior

(vertebrobasilar) circulation (Fig. 7.2).

A useful and simple clinical system for classifying stroke is

shown in Box 7.3.

Isolated vertigo, amnesia or TLOC are rarely, if ever, due

to stroke. In industrialised countries about 80% of strokes are

ischaemic, the remainder haemorrhagic. Factors in the history or

examination that increase the likelihood of haemorrhage rather

Anterior cerebral artery

Anterior communicating artery

Middle cerebral artery

Internal carotid artery

Posterior cerebral artery

Basilar artery

Posterior

communicating artery

Vertebral artery

Circle of Willis

Fig. 7.2 The arterial blood supply of the brain (circle of Willis).

7.3 Clinical classification of stroke

Total anterior circulation syndrome (TACS)

• Hemiparesis, hemianopia and higher cortical deficit (e.g. dysphasia

or visuospatial loss)

Partial anterior circulation syndrome (PACS)

• Two of the three components of a TACS

• OR isolated higher cortical deficit

• OR motor/sensory deficit more restricted than LACS (see below)

Posterior circulation syndrome (POCS)

• Ipsilateral cranial nerve palsy with contralateral motor and/or

sensory deficit

• OR bilateral motor and/or sensory deficit

• OR disorder of conjugate eye movement

• OR cerebellar dysfunction without ipsilateral long-tract deficits

• OR isolated homonymous visual field defect

Lacunar syndrome (LACS)

• Pure motor > 2 out of 3 of face, arm, leg

• OR pure sensory > 2 out of 3 of face, arm, leg

• OR pure sensorimotor > 2 out of 3 of face, arm, leg

• OR ataxic hemiparesis

124 • The nervous system

The physical examination

Neurological assessment begins with your first contact with the

patient and continues during the history. Note facial expression,

demeanour, dress, posture, gait and speech. Mental state

examination (p. 320) and general examination (p. 20) are integral

parts of the neurological examination.

Assessment of conscious level

Consciousness has two main components:

• The state of consciousness depends largely on integrity of

the ascending reticular activating system, which extends

from the brainstem to the thalamus.

• The content of consciousness refers to how aware the

person is and depends on the cerebral cortex, the

thalamus and their connections.

Do not use ill-defined terms such as stuporose or obtunded.

Use the Glasgow Coma Scale (see Box 18.5), a reliable and

reproducible tool, to record conscious level.

Meningeal irritation

Meningism (inflammation or irritation of the meninges) can lead

to increased resistance to passive flexion of the neck (neck

stiffness) or the extended leg (Kernig’s sign). Patients may lie with

flexed hips to ease their symptoms. Meningism suggests infection

(meningitis) or blood within the subarachnoid space (subarachnoid

haemorrhage) but can occur with non-neurological infections, such

as urinary tract infection or pneumonia. Conversely, absence of

meningism does not exclude pathology within the subarachnoid

space. In meningitis, neck stiffness has relatively low sensitivity

but higher specificity. The absence of all three signs of fever,

neck stiffness and altered mental state virtually eliminates the

diagnosis of meningitis in immunocompetent individuals.

Examination sequence

• Position the patient supine with no pillow.

• Expose and fully extend both of the patient’s legs.

Neck stiffness

• Place your hands on either side of the patient’s head,

supporting the occiput.

• Flex the patient’s head gently until their chin touches their

chest.

• Ask the patient to hold that position for 10 seconds. If

neck stiffness is present, the neck cannot be passively

flexed and you may feel spasm in the neck muscles.

• Flexion of the hips and knees in response to neck flexion

is Brudzinski’s sign.