Neurological disease

Chapter 22 Neurological disease

























































































Common symptoms and signs


Pattern recognition in neurology – interpretation of history, symptoms and examination – is very reliable. Practical experience is vital. There are three critical questions in formulating a clinical diagnosis:






Difficulty walking and falls


Change in walking pattern is a common complaint (Box 22.1). Arthritis and muscle pain make walking painful and slow (antalgic gait). The pattern of gait is valuable diagnostically.













Examination and formulation


Following a short or detailed examination, relevant findings are summarized in a brief formulation – the basis for investigation, transfer of information and management (Practical Boxes 22.1, 22.2 and Table 22.2).




Table 22.2 Six grades of muscle power
























Grade Definition

5


Normal power


4


Active movement against gravity and resistance


3


Active movement against gravity


2


Active movement with gravity eliminated


1


Flicker of contraction


0


No contraction




Functional neuroanatomy







Localization within the cerebral cortex


This subject causes unnecessary difficulty. Work on neuronal networks, functional imaging and plasticity questions the traditional views of highly specific localization of cortical function. The following paragraphs summarize areas of clinical relevance.





Aphasia

Aphasia is loss of or defective language from damage to the speech centres within the left hemisphere. Numerous varieties have been described.











Cranial nerves (Table 22.3)



I: Olfactory nerve


This sensory nerve arises from olfactory (smell) receptors within nasal mucosa. Branches pierce the cribriform plate and synapse in the olfactory bulb. The olfactory tract passes to the olfactory cortex.


Table 22.3 Cranial nerves



























































Number Name Main clinical action

I


Olfactory


Smell


II


Optic


Vision, fields, afferent light reflex


III


Oculomotor


Eyelid elevation, eye elevation, ADduction, depression in ABduction, efferent (pupil)


IV


Trochlear


Eye intorsion, depression in ADduction


V


Trigeminal


Facial (and corneal) sensation, mastication muscles


VI


Abducens


Eye ABduction


VII


Facial


Facial movement, taste fibres


VIII


Vestibular
Cochlear


Balance and hearing


 


Cochlear


 


IX


Glossopharyngeal


Sensation – soft palate, taste fibres


X


Vagus


Cough, palatal and vocal cord movements


XI


Accessory


Head turning, shoulder shrugging


XII


Hypoglossal


Tongue movement


Anosmia (loss of sense of smell) is caused by head injury (shearing of olfactory neurones as they pass through the cribriform plate at the skull base) or tumours of the olfactory groove (e.g. meningioma). Olfaction is temporarily (occasionally permanently) lost or diminished after upper respiratory infections and with local disorders of the nose. Many patients with gradual onset anosmia over many years may be unaware of the deficit, e.g. in Parkinson’s disease where anosmia precedes motor symptoms by many years but is often not noticed by the patient.


Detailed smell testing is difficult in routine clinical practice and rarely performed. Adequate testing requires use of commercially available kits such as scratch and sniff cards or odour filled pens with forced multiple choice identification.



II: Optic nerve and visual system (Fig. 22.4)


Light regulated by the pupillary aperture is converted into action potentials by retinal rod, cone and ganglion cells (see page 1055). The lens, under control of the ciliary muscle, produces the image (inverted) on the retina. Axons in the optic nerve (1) decussate at the optic chiasm (2), fibres from the nasal retina cross and join with uncrossed fibres originating in the temporal retina to form the optic tract (3). Each optic tract thus carries information from the contralateral visual hemifield.



From the lateral geniculate body, fibres pass in the optic radiation through the parietal and temporal lobes (4 and 5) to reach the visual cortex of the occipital lobe (6 and 7), which is somatotopically organized with macular vision located at the occipital pole (see Fig. 22.4).


Beyond the visual cortex visual information is further processed by neighbouring visual association areas to detect lines, orientation, shapes, movement, colour and depth; there is even a distinct area responsible for face recognition.




Visual field defects


Visual fields are assessed at the bedside by confrontation – comparing the examiner’s and patient’s fields, one eye at a time and quadrant by quadrant. Patience and good technique are required to get reliable results. White and red targets (traditionally hatpins) are used to assess peripheral and central fields respectively although in practice a fingertip is often substituted as a cruder screening test. More detailed quantification of fields may be obtained using Goldmann (manual) or Humphrey (automated) perimetry testing.


Field defects are described as hemianopic when half the field is affected and quadrantanopic when a quadrant is affected. Lesions posterior to the optic chiasm produce homonymous field defects, indicating involvement of the same part of the visual field in both eyes as information from the two visual hemifields is separated beyond this point. Lesions damaging decussating nasal fibres at the optic chiasm cause bitemporal defects.





Optic nerve lesions

Unilateral visual loss, commencing with a central or paracentral (off-centre) scotoma, is the hallmark of an optic nerve lesion. Because most fibres in the optic nerve subserve macular vision, lesions within the nerve disproportionately affect central vision and colour vision. A total optic nerve lesion causes unilateral blindness with loss of pupillary light reflex. Examination findings in optic neuropathy:



Causes are listed in Box 22.3.




Papilloedema

Papilloedema means swelling of the optic disc. Causes are shown in Box 22.4. The earliest signs of swelling are disc pinkness, with blurring and heaping up of disc margins, nasal first. There is loss of spontaneous pulsation of retinal veins within the disc. The physiological cup becomes obliterated, the disc engorged with dilated vessels. Small haemorrhages often surround the disc.



Various conditions simulate true disc swelling. Marked hypermetropic (long-sighted) refractive errors make a disc appear pink, distant and ill-defined. Myelinated nerve fibres at disc margins and hyaline bodies (drusen, p. 1064) can be mistaken for disc swelling.


Disc infiltration also causes a swollen disc with raised margins (e.g. in leukaemia).


When there is doubt about disc oedema, i.v. fluorescein angiography is diagnostic; retinal leakage is seen with papilloedema.


Papilloedema produces few if any visual symptoms other than momentary visual obscurations with changes in posture. The underlying disease is the source of the patient’s symptoms. The blind spot is enlarged but this is not noticed by the patient. However, over time progressive and permanent constriction of visual fields occurs, ultimately culminating in optic atrophy.









The pupils


A slight difference between the size of each pupil (up to 1 mm) is common (physiological anisocoria) and does not vary with differing light levels. The pupil tends to become smaller and irregular in old age (senile miosis); anisocoria is more pronounced. Convergence becomes sluggish with ageing.


Pupillary reactions to light and accommodation may be tested (Fig. 22.5). A bright torch (not an ophthalmoscope light!) should be used to test the pupillary light reaction.



Afferent pupillary defect. A complete optic nerve lesion causes a dilated pupil and an afferent pupillary defect (APD). For a left APD:



Relative afferent pupillary defect (RAPD). This occurs with incomplete damage to one optic nerve relative to the other. An RAPD is a sensitive sign of optic nerve pathology and can provide evidence of an optic nerve lesion even after recovery of vision. For a left RAPD:









III, IV, VI: Oculomotor, trochlear and abducens nerves


These cranial nerves supply the extraocular muscles and disorders commonly result in abnormal eye movements and diplopia (double vision) due to breakdown of conjugate (yoked) eye movements. Diplopia may also occur with local orbital lesions or myasthenia gravis.





Abnormalities of conjugate lateral gaze


A destructive lesion on one side allows the eyes to be driven by the intact opposite pathway. A left frontal destructive lesion (e.g. an infarct) leads to failure of conjugate lateral gaze to the right. In an acute lesion the eyes are often deviated to the side of the lesion, past the midline and therefore look towards the left (normal) limbs; there is usually a contralateral (i.e. right) hemiparesis.


In the brainstem a unilateral destructive lesion involving the PPRF leads to failure of conjugate lateral gaze towards that side. There is usually a contralateral hemiparesis and lateral gaze is deviated towards the side of the paralysed limbs.





Nystagmus


Nystagmus is rhythmic oscillation of eye movement, and a sign of disease of the retina, cerebellum and/or vestibular systems and their connections. Nystagmus is either jerk or pendular. Nystagmus must be sustained within binocular gaze to be of diagnostic value – a few beats at the extremes of gaze are normal.



Apr 1, 2017 | Posted by in GENERAL & FAMILY MEDICINE | Comments Off on Neurological disease
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