chapter 2
The Neurological History
This chapter will endeavour to provide a basic understanding of the principles of history taking so that the time spent on the ward learning how to take a history can be more effective, more interesting and more enjoyable. In particular, the pivotal aspects of clinical neurology will be discussed.
• Where is the lesion? Is the problem in the cerebral hemispheres, brainstem, cerebellum, spinal cord, nerve roots, brachial or lumbosacral plexus, peripheral nerve, neuromuscular junction or muscle? When considering the nature (i.e. whether it is weakness, sensory symptoms or visual or speech disturbances) and the distribution of the weakness and sensory symptoms in terms of which parts of the body are affected, thinking about the underlying neuroanatomy will help to localise the problem within the nervous system.
• What is the pathology? Establish the mode of onset and progression of the illness.
and family history of migraine was used to make a diagnosis of migraine. This patient’s symptoms were of instantaneous onset and were related to a ruptured berry aneurysm causing subarachnoid haemorrhage (bleeding into the subarachnoid space – the space beneath the outer lining of the brain, referred to as the dura mater, and the surface of the brain).
A past history of a medical problem does not preclude the patient suffering from
• A past history of an illness or risk factors for an illness only increase the likelihood that the patient has a particular problem; they should not be used to make a diagnosis.
• The nature and distribution of the symptoms can only localise the problem within the nervous system and cannot infer a particular pathological diagnosis.
a totally unrelated illness. The approach of using the past history to influence the diagnosis of the current problem often leads to a delay in diagnosing new problems in patients with chronic diseases. In most instances ‘prior probability’ is correct, and this can lull clinicians into thinking that they are clever when in fact it was difficult for them to be wrong even if they did not obtain a detailed history. Typical examples of this are an older person with a hemiparesis with the most likely cause being a stroke and the general practitioner (GP) who diagnoses most patients as having a tension-type headache and is correct the vast majority of the time simply because most patients attending a GP with headache do in fact suffer from tension-type headache.
Spencer [1] stated that it is not possible to learn how to take an effective history from a textbook. The clinical environment is the only setting in which the skills of history taking, physical examination, clinical reasoning, decision making, empathy and professionalism can be taught and learnt as an integrated whole. Although this is correct, one could use the analogy of learning to play golf: you can either hack away for years to teach yourself or you can have lessons that will make the practice more effective.
Traditionally, students have been taught to ask a long list of neurological questions about headache, dizziness, weakness, numbness etc in the forlorn hope that, after this ‘fishing expedition’ (also referred to as ‘looking for the pony’1) [2], a diagnosis will be apparent. In other words, in the hope of finding the diagnosis (‘the pony’), one collects a large list of answers to numerous specific questions that largely relate to the nature of the symptoms with little understanding about what the answers represent. It has been suggested that students should be taught to take a history this way and then taught not to take it that way. I disagree. I would like to recommentd that students should be taught how to take a history in a way that is meaningful to them rather than just collecting useless information they do not know how to use.
PRINCIPLES OF NEUROLOGICAL HISTORY TAKING
An alternative method of obtaining the history in patients presenting with intermittent disturbances of neurological function or recurrent episodes, e.g. epilepsy or headache, is recommended. In essence, with intermittent disturbances it is better to obtain a blow-by-blow description of several individual episodes. This alternative approach is described in Chapter 7, ‘Episodic disturbances of neurological function’ and Chapter 8, ‘Seizures and epilepsy’.
1. Define the likely underlying pathological basis by eliciting the mode of onset, progression and duration of each and every symptom (i.e. the time course of the illness).
2. Establish the site of the disorder within the nervous system by determining the nature and distribution of symptoms.
3. Elicit other facts that may either establish a cause for the problem or, more importantly, influence subsequent management of the patient. This includes the family history, past history, coexistent medical problems, prescribed drugs and natural remedies the patient is taking, social factors and the patient’s concerns.
THE UNDERLYING PATHOLOGICAL PROCESS: MODE OF ONSET, DURATION AND PROGRESSION OF SYMPTOMS
Different pathological processes evolve over variable periods of time and it is this variability that can be used to determine the most likely pathology. Three modes of onset can be loosely defined: sudden onset within seconds to minutes, gradual onset over hours to days and a very gradual onset over months to years (see Figure 2.1). The expression ‘mode of onset’ refers to the time for all symptoms to FULLY develop in terms of either their intensity and/or their distribution.
The pathological processes that reflect these modes of onset are:
A Instantaneous – seconds, rarely minutes
• Electrical: an epileptic seizure or an arrhythmia such as a tachyarrhythmia (fast heart beat), bradyarrhythmia (slow heart beat) or complete heart block (no impulse between the right atrium and ventricles, the Stokes–Adams attack)
• Vascular: subarachnoid haemorrhage, cerebral embolus
• Mechanical: trauma, a slipped intervertebral disc or positional vertigo
• Infective: meningitis, encephalitis
• Inflammatory: multiple sclerosis, acute inflammatory neuropathies
• Neoplastic: benign and occasionally malignant tumours
• Degenerative: cervical spondylitic myelopathy and the various genetic disorders
• Chronic endocrine problems: hypothyroidism, Cushing’s disease, pituitary disorders
• Chronic inflammatory/infective processes: polymyositis, chronic inflammatory demyelinating peripheral neuropathies, cryptococcal or tuberculous meningitis
Exceptions to the rule include:
• Symptoms such as diplopia (double vision) and vertigo will, as a result of their very nature, always begin abruptly and need not necessarily indicate a pathological process with a vascular or mechanical basis (see the section ‘The nature and distribution of symptoms’).
• At time, neoplastic disorders can present with a very rapid evolution of symptoms as a result of a seizure and the rapid onset of a focal neurological deficit after the seizure; tumours can also appear to evolve more rapidly when there is a superimposed mechanical shift due to the mass effect.
• Vascular disorders can have a slower onset: for example, the stroke-in-evolution that may or may not be stepwise; the intracerebral haemorrhage that evolves over many minutes; the subdural that develops over hours to days (although here the bleeding results in a mass lesion); or the giant aneurysm that behaves as a tumour with symptoms due to the mass.
• In older patients with a chronic disease the deterioration is so slow that it is assumed that their increasing disability is simply related to old age until there is a sudden crisis, such as a fall where they are unable to get up. Patients present under these circumstances with an apparent illness of sudden onset, where in reality it is simply the ‘straw that broke the camel’s back’ phenomenon. The true nature is only clarified when a careful and detailed history of slowly evolving disability is obtained.
There are two circumstances where it is not possible to establish the exact time of onset of the initial symptom(s):• Firstly, if the symptoms are present on awakening, even if the patient awoke at an unusual hour, unless you can determine that the symptoms awoke the patient (and this is very unlikely). The best estimate for the onset is the time between falling asleep and awakening.
• Secondly, if the symptoms are only noticeable when there is an external stimulus (e.g., the patient becomes aware of numbness only when they touch their face).
