APPROACH: WHERE IS THE LESION, WHAT IS THE LESION?
Exam - localising with clinical signs
This section is about the purpose and logic of the neurological examination, and its role in localisation.
Firstly, a key point: there are so many examination manoeuvres that there is no such thing as a ‘complete neurological examination’ - it is tailored to the problem being assessed.
The exam serves several purposes:
This site is dedicated to localisation so I will not focus on the other aspects.
Testing hypotheses during the exam
When we examine we already should have one or several hypotheses in mind, generated during the history. We look for evidence to confirm or refute these - ideally, ‘narrowing it down’ to one or a few likely explanations, which we then use investigations to confirm/refute. I cannot stress enough the point that bypassing this clinical process and simply doing tests is not only lazy and inefficient, but also causes all sorts of issues (summarised elsewhere). The clinical formulation is the anchor, guiding the investigations.
As an example - in a patient with bilateral leg weakness sparing the arms and cranial segment (i.e. paraparesis), the differential includes the following:
The best way to localise is via reflexes. If brisk, it suggests a UMN lesion, and if reduced/absent it points to an LMN issue (bar in the hyperacute phase of UMN lesions). We can then look for clues that distinguish the other lesion sites listed above, for example sphincter disturbance (cauda equina), co-existing sensory loss in a length-dependent manner (neuropathy), fatiguability (NMJ) or proximal predominance with no sensory features (myopathy).
However, sometimes we may not know exactly what the deficit is based on the history, if multiple options exist - so the exam can help this. For example, a patient with difficulty using a hand may have weakness, numbness, ataxia, apraxia or something else - the exam can then identify the true cause by testing various aspects of function.
It is best to have a standard 'routine' structure for most situations and to be able to customise to the problem. A routine examination should include cranial nerves, limbs (tone, power, reflexes, coordination and basic touch sensation), gait and stance. A general sense of cognition should be apparent through the history and the patient’s ability to follow instructions.
Depending on the situation, we may include other elements which are not ‘routine’ but help us make a diagnosis. Examples include:
Some settings call for a standardised sequence that determines treatment based on a score. The best-known is the National Institute for Stroke Score (NIHSS), a rapid sequence that screens for major deficits caused by to stroke, not only allowing localisation but also enabling decision-making around reperfusion therapies. It includes tests for major weakness in the proximal muscles in each limb affecting anti-gravity strength, rather than looking at individual muscles in depth, and it ignores things which have no relevance in hyperacute stroke (such as reflexes).
In contrast, examination of a suspected peripheral problem can require a detailed examination of muscles to map the lesion precisely. If doing this for an upper limb issue such as difficulty with fine movements in one hand, the examiner would carefully examine the affected region to help find the cause - for example ulnar neuropathy, T1 radiculopathy or even a motor homunculus lesion. The process would include testing different muscles innervated by various roots and nerves to find the lesion.
We will look at some specific situations in more detail now. Many of the cases in this site give examples of these.
Sensory loss
Sensory complaints are very common and many reflect benign causes, especially if the symptoms fluctuate and are not there constantly. However, serious disorders can produce persistent sensory disturbance. Our task is working out if symptoms reflect a secondary cause and if so, where and what the lesion is.
The key is mapping the affected region and testing which modalities are involved. Then we can consider possible anatomical explanations. These follow rules outlined in the Where? section.
Brain lesions often affect the contralateral hemi-head and body, although can be more focal if in the sensory cortex (unless large). Cortical lesions may also produce higher-order sensory abnormalities such as agraphaesthesia and astereognosis even if primary sensation is spared.
Thalamic lesions can produce a variety of patterns, including complete hemihead/-body ‘splitting’ but also more unusual distributions such as cheiro-oral syndrome.
Brainstem lesions tend to cause crossed signs, with ipsilateral cranial region sensory loss, and contralateral body sensory loss. The modalities involved depend on the lesion; for example lateral medullary lesions affect the spinal trigeminal and spinothalamic tracts, so alter pain and temperature sensation but spare other modalities.
Cord lesions vary with the lesion level and also side, site and size in the cord, hence the modalities involved depend on this, and patterns vary, as was discussed in Where?. Finding the sensory level is important, and the lesion is typically at or slightly higher than this. If the arms are involved the lesion cannot be lower than the high thoracic cord, although the opposite isn't true - lesions higher than this can sometimes spare the arms, and can be missed if we omit this region on imaging in someone who only has lower limb (and perhaps torso) symptoms.
Lesions in the periphery vary.
Polyneuropathy features glove-and-strocking sensory loss, so if the sensory loss goes to the thighs and spares the hands this suggests a more central cause.
Root, plexus and mononeuropathy lesions will affect a specific distribution in a region of skin, so we need to map this out. These regions may overlap (for example L5 and common peroneal nerve), and it can be difficult to be sure of the lesion site, so other features such as weakness (if present) help this.
The most difficult lesions to site involve smaller areas. It is generally easier the more extensive the sensory loss, e.g. all 4 limbs or entire hemibody. One presentation which is difficult is sensory loss to the mid-shins, which can be polyneuropathy or lesion in the cauda equina or cord - the presence of additional signs such as wasting, weakness or reflex changes may help, but with such distal abnormalities it can be hard to know entirely where the lesion is.
Weakness
The approach taken to localising weakness is similar to sensation, and the key is first mapping affected regions - a lesion may be anywhere in the motor tract between its cortical origins and target muscle groups. The same patterns apply as in the sensory section, for example partial or total head and body weakness on the opposite side with brain lesions - with the exception that some areas have bilateral UMN supply so are not weakened by a unilateral lesion (e.g. forehead elevation). The same patterns apply for brainstem (crossed signs), spine (motor and sensory level) and other regions.
Other features that help are tone and reflexes, in terms of separating UMN versus LMN, as above. However, brisk reflexes due to UMN pathology can take time to develop. They are helpful if seeing someone several days or weeks into a problem, as we might in a clinic - but not necessarily discriminatory in the first days, for example in an acute presentation leading to hospitalisation.
Sensory features, if also present, can be helpful clues in localising weakness. In an anterior spinal artery infarct there is generally loss of spinothalamic modalities bilaterally but sparing of the dorsal column functions, and there should be a sensory level in the trunk - this helps differentiate from other causes of flaccid paraplegia such as cauda equina syndrome. Another example would be a weak leg with contralateral spinothalamic modality loss due to a lateral cord lesion - this pattern is highly suggestive, and doesn't reflect pathology anywhere else.
Other clues from distribution were explored in Where? - such as prominent ocular, facial and bulbar features in NMJ disorders, proximal weakness in myopathy, and distal predominance in neuropathy.
Visual problems
The visual pathways start in the eye and work back through the optic nerves, chiasm, optic tracts, thalamic synapse, then the two radiations until terminating in the occipital cortex. Localisation is possible based on the features - monocular vs binocular, and what part of the hemifield is affected on which side.
There is then a complex system of higher-order visual processing distributed between the occipital, parietal and temporal lobes. Lesions here cause more complicated effects rather than primary visual loss, for example issues perceiving movement or recognising faces. Small, focal lesions can produce isolated deficits such as this.
When we examine our task is to find out what the problem is and where the pathology may lie. We can test acuity, fields, examine the optic disc, test pupillary light and accommodation reflexes and assess colour vision. Examining the blind spot is also helpful.
Note that 'blurred vision' reported in the history may be due to problems other than visual acuity loss. Nystagmus may also produce it due to constantly disrupted foveal fixation amid eye moveents. Diplopia (e.g. due to a VI palsy) may be reported as ‘blurred’ vision too, and the opposite is true - altered acuity may blur outlines, being perceived as 'double vision' - without truly seeing two separated images.As with all examination, this requires solid technique to minimise risks of artefacts. The patient must be clear what they are being asked to do, and we need to clarify what they are experiencing if an abnormality is identified.
If the patient is confused, dysphasic, agitated, drowsy or otherwise has altered ability to interact, it becomes difficult to meaningfully assess vision and we resort to basic measures such as testing each hemifield with a threat stimulus (a hand quickly brought towards their face) to see whether they blink - a common test in hyperacute stroke patients - and pupillary reflexes.
Vertigo
Vertigo is common. Localisation is split between the vestibular system in the ear and nerve VIII (peripheral) and associated structures within the brain and cerebellum (central).
In persistent vertigo, if there are obvious features of a central lesion such as hemi-ataxia or sensory loss then localisation to a central cause is straightforward, and we then localise it further using the principles described earlier, for example cross-localising with other signs (e.g. suggesting damage in lateral medullary structures).
If such features are not obvious then we have to look in more detail. Eye signs are the most informative, and if there is nystagmus, its characteristics can discriminate. 'Peripheral' nystagmus is horizontal and may have a torsional component, and the direction of the horizontal fast phase doesn’t change whichever side the patient looks. Anything else is central. We can also test the vestibulo-ocular reflex (VOR) by head impulse testing to see if the eyes can fix on a target despite rapid head movements. If altered, the problem is peripheral - which is usually reassuring. People with peripheral vertigo can also usually walk unaided, even if it feels unpleasant and they are a bit unsteady. If they can't walk or stand without support the cause is usually central.
In episodic vertigo the patient may be asymptomatic at rest, so we use provocative manoeuvres to see if we can trigger an attack. These test the three semicircular canals and allow localisation of the cause - nystagmus appears with vertigo. We can follow a positive test with a corrective manouevre to treat the problem.
Cognitive problems
Cognitive problems are very common, and by testing the various cognitive domains (e.g. memory, executive and visuospatial functions) we can localise the cause within the brain.
We can formally test cognition using psychological tests, but bedside tests of cognition, and other tests relevant to the various brain lesions, are also helpful. Even before this, cognitive performance is evident during the history, and we may spot lots of issues with language, memory, attention and organisation of thought processes. The history from an informant is also very revealing - many people with cognitive problems lack awareness of their presence and extent (anosoagnosia).
Frontal lobe functionsThe frontal lobe has many roles, including problem solving, complex decision-making and reasoning, language, and social functions including empathy. Damage has drastic consequences on cognitive and social functioning.
We may note unusual social behaviours, such as a lack of interest in the consultation, an inappropriately jolly or joking manner, a tendency to interrupt rather than observing natural turns in conversation, and to make insensitive remarks (as if the person has 'lost their filter'). People often struggle to keep up with the flow of the assessment and may appear to get stuck on a subject or task that has already concluded (perseveration).
People struggle with abstraction, such as explaining the meaning of proverbs or similarities between discrete objects (e.g. knowing that a banana and orange are both fruit). They also struggle with tasks of fluency - generating as many words as possible in a minute according to a rule (e.g. beginning with a letter, or belonging to a category such as animals) - despite having fluent speech. In such situations the problem is not a primary language one but the ability to perform a strategic goal-directed task under pressure.
Utilisation behaviour may be evident - picking up items around the room and using them without any instructions to do so, for example a pen and paper on the desk.
Frontal release signs are primitive features seen in infants that re-emerge with frontal lobe damage - the pout, root, snout, grasp and palmomental reflexes.
Parietal lobe functionsThese include numeracy and visuospatial functions. We can ask people to do simple arithmetic, or to draw objects such as a flower or clock. Problems might include asymmetrical drawings suggesting neglect - e.g. a clock with all the numbers on one side - or frank inability to draw anything (constructional apraxia).
There may be problems with praxis, for example copying gestures or miming an action most people would know (turning a key in a lock, brushing teeth, putting on a hat) - in the absence of weakness or ataxia.
Visual or sensory inattention may also be evident in parietal disease so is worth testing, likewise checking for a cortical sensory deficit.
Temporal lobe functionsMemory is important to test. We can ask about recent events in the news, or the patient’s overall awareness of their illness. These reflect long-term memory, even though they're recent developments - and problems suggest an issue with generating and storing new memories for later retrieval.
We can also directly test ability to make new memories. We can give people a short piece of information to remember, such as 3 items (lemon - key - ball) or an address. We test immediate recall (‘repeat after me…’) to see if they are able to take this information in and repeat it. Then we test delayed recall after an interval - to see if the person can convert the new information into long-term memory. Intact immediate recall with impaired delayed recall is characteristic of dysfunction in the hippocampus and its outflow system. Poor immediate recall is more suggestive of issues with attention, which can manifest as 'poor memory'.
Putting it all together...
Having taken a careful history, thought about the symptoms and what site and process they may map to, then examined to support our suspicions - we can now attempt a clinical formulation of the patient's problem.
Clinical Formulation