ALS News & Research For postings of news or research links and articles related to ALS


advertisement
Reply
 
Thread Tools Display Modes
Old 10-03-2007, 05:39 AM #1
BobbyB's Avatar
BobbyB BobbyB is offline
In Remembrance
 
Join Date: Aug 2006
Location: North Carolina
Posts: 4,609
15 yr Member
BobbyB BobbyB is offline
In Remembrance
BobbyB's Avatar
 
Join Date: Aug 2006
Location: North Carolina
Posts: 4,609
15 yr Member
Post How to do a neurological examination in five minutes or less

How to do a neurological examination in five minutes or less
02 Oct 07

What kind of neuro exam can GPs be expected to do in a brief consultation? Probably a fuller one than you think, argues neurologist Dr Giles Elrington

Neurology and the neurological examination is traditionally considered to be difficult. In fact, neurology is quite simple and the examination is subject to logic and is, with practice, quick and easy.

The main challenge is that the ‘full neurological examination’ is not practicable in routine clinical practice. Unlike the cardiovascular, respiratory or abdominal examination there is no one-size-fits-all and the neurological examination must be tailored to the individual patient and the problem they present.


It’s like driving
Some parts of the examination are technically challenging and therefore require practice – like learning to drive. Just as few of us drive as we did for the driving test, few neurologists ever perform a full neurological examination.

It would simply take too long – perhaps 10 minutes for cranial nerves, 15 minutes for limbs and trunk, and several hours for cognition. The standard NHS appointment for a new patient is 30 minutes, longer than a GP consultation but not long enough to do everything.

Another parallel with learning to drive is the practice of the individual skilled parts. You would never learn to parallel park or to do a three-point turn if you only ever did it when you had to. Similarly, the tendon reflexes – especially the left ankle jerk, fundoscopy and visual fields – require repetitive practice.

So if you are unhappy about fundoscopy, for example, taking a quick look at the optic discs of everyone you see over a week or two will bring both confidence and experience of the range of normality. Don’t worry if sometimes you can’t see what you want, this will become easy in time.

Like driving, many (male) neurologists seem to think the way they do it is the best and everyone else is wrong. Actually we all find a way that works for ourselves, but when errors or near misses happen – and they happen to everyone – we have to learn to improve.


Why not just do a scan?
Some doctors appear to skip the neurological examination and rely on a combination of history and investigation – usually an MRI scan. This results in over-investigation and many ‘incidentalomas’ on MRI scans. MRI scanning is like fishing with a fine mesh net – you catch a lot of useless small fry.

Neurologists spend an increasing amount of clinic time reassuring people with benign symptoms and incidental findings on pre-referral MRI. There are, however, some helpful shortcuts for the non-examiner – for example, an optician can diagnose papilloedema, or visual field loss.

Possibly abnormal findings on examination need to be considered carefully and in context. It is always best to rely not on one but on many findings which fit the clinical problem suggested by the history.


The examination
The examination is divided into cognition or higher mental function, cranial nerves, central nervous system (CNS) and peripheral nervous system. Contrary to popular belief the CNS is not just the head, and in ‘medical clerkings’ must be distinguished from the ungrammatical ‘CN’s’ for cranial nerves.


Cognition
Where there is no complaint of cognitive problems and the patient appears to behave normally and give a consistent history, cognitive examination is not indicated.

Patients who present alone with subjective memory loss, and no account of disaster in daily life, rarely have a neurological diagnosis. Stress is the usual cause.

Asking ‘are you depressed or anxious?’ is about as useless as asking what they think their cholesterol level might be: inquiry about sleep patterns, feeling more tired in the morning than the evening, loss of enjoyment, plans for the future, are more helpful.

Using a standardised rating scale such as Beck can be very useful.

Features suggestive of cognitive impairment include evidence of abnormal behaviour, inability to give a history, and concern from relatives or employers. Step one is to assess attention, which if impaired precludes all other cognitive tests and when acute suggests a confusional state which is usually caused by infection or metabolic disturbance including drug toxicity.

Formal assessment of attention is assessed by asking the patient to count backwards from 20 to zero: success at this task excludes attention problems.

Next, test for dysphasia: show your watch, what is this? What are the things that move round and point at the numbers? What is this knob on the side? What is this that holds it on my wrist? What is this that holds the strap together?

A fountain pen is another useful object: do not use body parts, your clothes, or random embarrassing things that you happen to have in your pockets.

If you suspect dementia, use a standardised screening test such as the MMSE. A score of 28/30 or more effectively rules out Alzheimer’s disease.


Cranial nerves
As a medical student you may have learnt a sexist mnemonic for nerves I-XII. Do not share this with the patient and do not go through the nerves in order. I only know one neurologist who routinely tests smell and that’s because it’s his research interest.

Visual fields are not really part of the cranial nerves but are conveniently considered here. In routine practice test both eyes together, in four quadrants – ‘south-east, south-west, north-west, north-east’.

A common abnormality is a homonymous hemianopia where the patient sees nothing to one side. Other field defects are so rare as not to worry about except in special cases, for example bitemporal hemianopia in chiasmal (such as pituitary) lesions, altitudinal monocular hemianopia in retinal vascular occlusions or scotomas in retinal disease. Detailed testing requires formal perimetry, or the use of a red pin which are not matters for primary medical care. Most hemianopias are caused by stroke, and are a bar to driving.

Occasionally it is worth testing visual acuity, one eye at a time, using reading glasses. If normal newsprint can be read there is no great problem.

Eye movements are important and must not be overlooked. Textbook III IV and VI palsies are the least common abnormalities. VI is usually vascular; III is urgent if painful and the pupil is widely dilated; forget about IV in primary care.

The common significant abnormalities are jerky eye movements and nystagmus which imply brainstem disease. Impairment of upgaze is always significant, though together with other disordered eye movements is often caused by cerebrovascular disease in older people and may not be clinically significant.

Test facial movement by asking patients to screw up their eyes and grin. Test facial sensation in forehead, cheek, chin (ophthalmic, maxilliary mandibular branches of III) and perhaps corneal reflexes, but look for contact lenses first.

Look at the tongue; it should protrude centrally, and not be wasted. If you fear motor neurone disease, all active tongues may appear to fasciculate, so distract the patient by asking them to say ‘aah’ while you pretend to look at the palate, while actually inspecting the tongue.


Central nervous system
This is the main – and often only – part of the routine brief neurological examination. I give a suggested ritual examination, which includes some cranial nerves (see box, below??).

This is the examination I do for patients with headache and with possible epilepsy – which make up at least half of all new referrals. Most of this is done with the patient standing. The only clothes removed are shoes.


Peripheral nervous system
This is my suggested screen. When symptoms suggest a specific nerve or root lesion, these require further specific tests.

Tendon reflexes are normally absent (or diminished) in cases of neuropathy. In this context it is worth remembering how to record the tendon reflexes:

Pathologically brisk +++
Brisk normal ++
Sluggish normal +
Present with reinforcement ±
Absent even with reinforcement-
Sensation: vibration sense in the big toe is normally lost in neuropathies; additionally there may be a sensory gradient to distal pinprick sensation.


Physical signs to forget?
There are some neurological signs that mean very little in isolation and are best disregarded in primary care. Isolated sensory signs are rarely relevant. The only time sensory examination is really important is in the demonstration of normal sensation in cases of possible motor neurone disease. Otherwise don’t bother to screen sensation in detail.


Muscle power is actually more difficult to assess than it might seem. Patients complaining of weakness tend to reproduce their symptoms when examined; what you need to do is to demonstrate a pattern of weakness such as pyramidal, radicular, specific peripheral nerve, proximal, distal.

Global weakness is rarely caused by organic disease. The MRC scale of weakness (grades 1-5) is diagnostically unhelpful, most weakness being grade 4 (against resistance). For quick testing in primary care it is better to focus on reflexes and muscle tone.

The glabellar tap is sometimes erroneously thought to help in the diagnosis of Parkinson’s disease: it is, like other primitive reflexes, of no relevance except in specific cases of neurodegeneration or frontal mass lesions.

‘Intention tremor’ is a confusing and misleading term, which used correctly implies cerebellar ataxia of the arm, not a tremor.

‘La belle indifference’ was a term used to describe an apparent lack of concern shown by some patients towards their symptoms. It was thought to imply hysteria, an outdated and pejorative term for what later became known as somatisation but is now properly called ‘medically unexplained symptoms’, a condition seen in a third of new neurological referrals.

Unhelpful terms abbreviations must be avoided: like quasi-humorous terms such as ‘NFN’ they diminish confidence and professionalism when read by patients or, worse, by their lawyers.

• NAD: does this mean ‘no abnormality detected’ or ‘not actually done’?

• Gross is not a useful term (such as grossly normal; grossly NAD). Either say normal, or leave it out.

• Focal is a redundant word, intended presumably to impress the layman, of no clinical value: all neurological signs are focal.

• Equivocal is an unhelpful term. If you’re unsure, go back and assess the sign again, or set it aside.



Specific clinical scenarios
These are given in approximate order of commonness.

Acute headache: look for rash and for meningism. In first, worst or thunderclap headache lasting up to an hour the absence of physical signs does not preclude the need for investigation.

Chronic headache: abnormal physical signs are not expected, use the CNS screen above paying particular attention to the possibility of papilloedema.

Seizures, attacks and funny turns: the history is critically important. This must be taken from the patient and from a witness. Examination is usually unhelpful, but use the CNS screen above, also carefully examine, and perhaps investigate, the cardiovascular system.

Carpal tunnel syndrome: this is the common cause of a numb tingly hand. Tinel’s test at the wrist is not the most specific test. Look instead for a pinprick gradient from finger to palm in the index finger. The tendon reflexes should be normal, no Horner’s syndrome and usually no weakness in the hand. Any weakness should be confined to abductor pollicis brevis, affected only in severe cases.

Bell’s palsy: the upper and lower face should be approximately equally affected. Lower face alone is more likely to be an upper motor neurone lesion in which case there are often other upper motor neurone signs in the limbs, sometimes cognitive impairment such as dysphasia with a right (dominant) facial weakness. Facial sensation, corneal reflexes and eye movements should be normal, no deafness and no ataxia.

Dizziness: this examination strategy is for vertigo, an illusion of movement – the history should distinguish vertigo from unsteadiness or anxiety. The common cause is vestibular disease, which may cause nystagmus at rest though this is often seen only with Hallpike’s manoeuvre where the patient lies on their back with the head down below the horizontal, and rotated to one side.

In peripheral vestibular disease this triggers the symptom, with nystagmus, after a delay of a couple of seconds; and repetitive testing fatigues the response. In cases of vestibular disease there should be no other abnormal signs on CNS and cranial nerve screen.

Sciatica: this is a lumbar radiculopathy caused by disc prolapse, causing pain all the way to the foot, not just to the knee. Straight leg raising should be impaired with a positive stretch test; the ankle jerk diminished, plantar not extensor, weakness around the ankle and sometimes also of hamstrings. Sensory loss in distal leg, not in thigh or perineum.

Multiple sclerosis: CNS signs are required for the diagnosis. No signs at peak of symptoms excludes MS. The abdominal reflexes are usually absent. There are usually some of the following: pale optic disc(s), afferent pupillary defect, visual loss, disordered eye movements of which an internuclear ophthalmoplegia (‘medial rectus palsy’, that is slowness or failure of adduction) is almost pathognomonic; spastic paraparesis; cerebellar ataxia. The diagnosis of MS can never be made at the first attack.

Parkinson’s disease: tremor is absent in a third of cases. Bradykinesia (slowness and poverty of movement) is the essential clinical feature. Asymmetry is almost invariable. Other physical signs are diminished ‘piano playing’ movements where the fingers move together not individually and cogwheel rigidity – the ‘ratchet effect’ – at the wrist enhanced by movement of the opposite arm.

A sustained response to levodopa with the later emergence of l-DOPA induced dyskinesia, and/or cognitive impairment with hallucinations of people and animals effectively confirms the diagnosis.

Tremor: rest tremor is seen in Parkinson’s disease (PD), though is neither specific nor essential for the diagnosis. Action or postural tremor does not suggest PD but is usually a benign essential tremor. The tremor is best seen with the arms outstretched; there may be head tremor (titubation), not the isolated jaw tremor of PD. Spiral drawing is corrupted, there handwriting is large and messy unlike PD micrographia.

Cerebellar disease presents not with tremor but with clumsiness. The eye movements are abnormal.

Stroke: this diagnosis requires the abrupt onset of CNS impairment. There is normally a hemiparesis with increased tone, pathologically brisk reflexes and an extensor plantar. ‘Weakness’ is not enough, there must be a pyramidal distribution of weakness such as arm extensors and abductors weakest, leg flexors and adductors weakest; face: upper spared, lower weak. Stroke is diagnosed on clinical grounds, not from a brain scan as MRI always shows ischaemia in arteriopaths and in older people.

Diffuse cerebrovascular disease: this is a common cause of gait disturbance in older people and in arteriopaths. The term ‘vascular pseudo-parkinsonism’ is inappropriate as it has nothing to do with PD, and it isn’t pseudo. The gait is short stepping, wide based and clumsy, with unsteadiness on turning.

Signs are relatively symmetrical, eye movements jerky with poor upgaze, and cognition may be impaired. This contrasts with PD where the short-stepping gait is narrow-based, turning causes freezing not unsteadiness, symptoms and signs are asymmetrical, are worse in arm than leg, eye movements normal, and cognition usually normal at initial presentation.

Cognitive impairment: mood disorders commonly mimic dementia, though unexplain-ed new depression or anxiety in an older person may herald dementia. It is important to obtain a history from family or friends.

Alzheimer’s disease and vascular dementia (which often overlap) can be screened using the MMSE.

Lewy body dementia is often associated with PD, begins with forgetfulness, matures into sleep disturbance with formed visual hallucinations, and delusions. It varies from day to day and week to week. The MMSE is insensitive to this diagnosis.

Frontotemporal dementia (FTD) presents with behavioural change, often with little insight and no physical signs. The MMSE may be relatively normal. A subgroup of FTD is primary progressive aphasia which presents with a marked dysphasia and few other physical signs.

Spinal cord disease (myelopathy): this presents with a paraparesis (spastic legs), usually bladder impairment. If the problem is in the neck the arms are also affected (a tetraparesis). There are no signs above the neck. There is usually a pinprick level on the trunk, which may be falsely low in incomplete lesions. Asymmetrical myelopathies cause spasticity on one side and sensory loss on the other side.


Medically unexplained symptoms
The commonest sign is an unusually large set of notes containing many speculative, evidence-free diagnoses.

Hoover’s sign is helpful in non-organic leg weakness: in attempting to flex the hip, the contralateral leg fails to extend, even though extension can be achieved to command.

Straight leg raising is sometimes substantially impaired by pain from ‘sciatica’, yet the patient will happily sit upright on the examination couch with legs extended.


Conclusion
The CNS can be screened in only a couple of minutes. Specific neurological diagnoses suggested by the history should be targeted with focused examination. A ‘full neurological examination’ is rarely indicated.

Dr Giles Elrington is a consultant neurologist at Bart’s and The London NHS Trust, London


Suggested brief exam

-
• Gait: normal or abnormal? Walking aids
• Romberg’s test: feet together, eyes closed (be ready to catch if the patient falls). Remember that normal people wobble a bit doing this test.
• Walk on heels, on toes, then hop on each foot.
• Hold hands outstretched with palms up and look for drift. Eyes still closed; touch right middle finger and ask ‘touch your nose with this finger’; repeat with left index finger.
• Eyes open: play the piano; tap your hand…faster.
• Look at my face…point at the finger that moves (right lower…left lower… both together, upper – possible inattention.
• Follow my finger (eye movements).
• Screw up your eyes (look also for pupillary response on eye opening) then look at forehead for elevated eyebrow – possible Horner’s syndrome. Grin – show me your teeth.
• Lie on the couch…fundoscopy, tendon reflexes, plantars (pulse and blood pressure).


http://www.pulsetoday.co.uk/story.as...de=4114974&c=1
__________________

.

ALS/MND Registry

.
BobbyB is offline   Reply With QuoteReply With Quote

advertisement
Reply


Posting Rules
You may not post new threads
You may not post replies
You may not post attachments
You may not edit your posts

BB code is On
Smilies are On
[IMG] code is On
HTML code is Off


Similar Threads
Thread Thread Starter Forum Replies Last Post
Selegiline Transdermal System--examination of potential Pharmacokinetic Interactions olsen Parkinson's Disease 0 02-05-2007 01:54 PM


All times are GMT -5. The time now is 12:30 PM.

Powered by vBulletin • Copyright ©2000 - 2024, Jelsoft Enterprises Ltd.

vBulletin Optimisation provided by vB Optimise v2.7.1 (Lite) - vBulletin Mods & Addons Copyright © 2024 DragonByte Technologies Ltd.
 

NeuroTalk Forums

Helping support those with neurological and related conditions.

 

The material on this site is for informational purposes only,
and is not a substitute for medical advice, diagnosis or treatment
provided by a qualified health care provider.


Always consult your doctor before trying anything you read here.