Historia neurologica

1. SYMPTOMS AND SIGNS
Taking a neurological history
Angus Kennedy
Rasheed Zakaria
Abstract
A detailed neurological history allows the physician to determine where
the lesion is within the nervous system, the nature of the pathological
process, and which physical signs to look for when examining the patient.
Taking a good history requires a basic knowledge of the hierarchical orga-nization
of the nervous system and the principles of functional localiza-tion.
Characterizing the pattern of neurological disease over time is
important: episodic, fluctuating and progressive courses of symptoms
are the most common. A clear description of events before, during and
after an episode (from an eyewitness if necessary) is essential. Different
symptom complexes may point the clinician towards cortical, extrapyra-midal,
spinal, radicular, peripheral nerve and neuromuscular pathologies.
These presentations are discussed.
Keywords assessment; examination; history; neurological symptoms;
neurology
What is different about a neurological history?
Whether in general practice or a busy medical assessment unit,
the neurological history should be a focused, goal-directed
exercise that seeks to answer the following questions.
Which part of the nervous system is affected and where is
the lesion? Is it single or are there multiple lesions, or is
there a diffuse problem affecting many neurological
systems?
What is the underlying pathological process (e.g. inflam-matory,
vascular, infectious)?
Is this a purely neurological problem or a neurological
manifestation of a systemic disease?
A full neurological examination for every possible sign is not
always practical, and a clear history allows examination of the
relevant aspects. Collateral history from a relative or care-giver is
often helpful, particularly in cases of loss of consciousness or
where there has been a recent change in behaviour or cognitive
ability. Where possible, permission should be sought from the
patient before obtaining collateral history. Finally, whilst one
should always beware of ascribing symptoms to the ‘mind’ rather
than the ‘brain’ without full investigation, there is overlap of
neurology with psychiatry and one must always consider the
patient’s affect, mood and other psychiatric aspects during the
encounter.
Approach to the neurological history
A friendly and relaxed interview style should be adopted which
allows the patient to describe symptoms in their own words.
Open as well as closed questions should be used. Each symptom
should be carefully explored with regard to its severity and time
course, clarifying what the individual actually means by their
symptoms. You should try to understand how the individual’s
work, social life and emotions have been affected. If the history is
complex, a brief initial overview can be helpful to outline the
‘shape’ of the history. Often, patients find it difficult to describe
neurological symptoms. It is usually best to take the history in
temporal sequence, asking the individual to report the very first
symptoms and subsequent developments. Some useful questions
to ask in different situations are included in the last section of
this chapter.
Basic information
Age: the most likely cause for any particular symptom will vary
at different ages.
Handedness: almost all right-handed individuals and at least
three-quarters of left-handed ones are left-hemisphere dominant
for language and this information is important when localizing
a lesion. The more left-handed the patient is, the more likely they
are to be right-hemisphere dominant.1
Presenting complaint: the patient’s most troubling problem (e.g.
headache, loss of consciousness) is sometimes difficult for them
to identify, particularly if they have impaired insight. It is useful
to consider the evolution of the symptoms. Sometimes formu-lating
a list of problems can be helpful in clarifying their
sequence and importance. If they have an established diagnosis,
such as multiple sclerosis (MS), ask about the symptom that has
brought them to hospital, Can it be explained by their disease
process or not?
How have the patient’s symptoms and disease changed
over time?
Careful identification of any pattern of symptom progression is
important in differential diagnosis.
Discrete episodes
If a patient has episodes, such as seizures or blackouts, start by
asking about the most recent event. Structure the history clearly
under the headings ‘Before’, ‘During’ and ‘After’. Then try
drawing a simple chart of the episodes in time.
Describe each episode:
What was happening immediately before the episode?
(The circumstances sometimes help to determine the
aetiology.) What was the patient doing, and how did their
symptoms affect them?
Angus Kennedy MD FRCP is Consultant Neurologist at Charing Cross
Hospital, and Chelsea and Westminster Hospital, London, UK. His
interests include the diagnosis, investigation and management of
degenerative dementia. Competing interests: none declared.
Rasheed Zakaria MA BMBCh qualified from Cambridge University, and
Oxford University, UK, winning the prestigious Geoffrey Spray Hill prize.
He is currently on a Neurosurgical Training programme. Competing
interests: none declared.
MEDICINE 40:8 403 2012 Published by Elsevier Ltd.

2. SYMPTOMS AND SIGNS
In what position was the patient (lying, standing, seated)?
Were there factors such as sleep deprivation or alcohol
excess, which may have lowered the seizure threshold?
Do recurrent events always happen upon standing (sug-gesting
postural hypotension)?
In the case of vertigo, recurrence on turning the head or
sitting up from lying flat may indicate benign positional
vertigo.
The availability of thrombolysis for stroke means that the
time of onset of symptoms needs to be precisely noted.
What happened during the episode? Clarify the sequence
of events as demonstrated in Figure 1. Here an eyewitness
is invaluable, particularly if the patient loses conscious-ness.
In the case of possible seizures, ask about features
that may help their differentiation from syncope, for
example, triggering factors, the presence of presyncopal
symptoms (nausea, greying of vision, muffled hearing),
pallor and sweating, occurrence of tongue-biting, duration
of loss of consciousness, and the nature and duration of
the post-ictal phase. Incontinence and jerking movements
(brief in the case of syncope) may occur in either. Consider
also the possibility of psychogenic non-epileptic seizures.2
Pattern of episodes over time: If symptoms are recurrent, ask
about the timing of the first episode, and the periodicity and
duration of subsequent events. In the case of epilepsy it is helpful
to ask about the patient’s longest seizure-free interval. In
women, migraine or seizures may occur in association with
menstruation or ovulation.3,4
It is helpful to record this information in a methodical,
objective way as pictured in Figure 2. If the individual has had
multiple (10 or more) episodes of altered consciousness, one can
usually obtain a history of the first episode, the worst episode
and the most recent episode. If seizures have recurred after
a period of seizure freedom, possible causes should be sought.
When presented in this way it is clear that these episodes we re
at one stage entirely absent but then returned. Once this had been
established the clinician was able to go on and clarify what had
specifically changed at that point; in this case eating chocolate –
a migraine trigger – whereas the patient was previously on a diet.
Fluctuating levels of severity
Pathological processes, such as inflammatory or autoimmune
disease (common examples being MS or myasthenia gravis),
often present with episodic symptoms but with a longer time
frame. Patients may be asymptomatic between exacerbations.
The level of function at different time points, especially before
and after therapies, should be assessed. Useful questions include
the time taken to perform a certain task, how far the patient can
walk unaided or how many of the activities of daily living such as
washing and dressing they can perform alone. These factors are
often formalized in scoring systems, such as the expanded
disability status scale for MS5 or the more general Barthel index.6
If myasthenia is suspected, the patient should be quizzed about
fatigability, whereas in multiple sclerosis, symptoms may be
more pronounced in summer or after a hot bath (Uhthoff’s
phenomenon). The pattern of symptoms in MS is particularly
important in determining the nature of the disease (e.g. primary
progressive, relapsingeremitting (as demonstrated in Figure 3)
or secondary progressive).7 This directly affects choice of thera-pies
that are available.
Progressive disease
Other neurological diseases are progressive: examples include
Alzheimer’s disease and motor neurone disease (MND). Some
degenerative conditions may be susceptible to treatments that
delay progression (Figure 4), but these rarely reverse the under-lying
disease process.8 It is important to determine the speed of
symptom progression in order to plan management. When did
symptoms first appear? How quickly has function been lost? In
MND, for example, how many different parts of the motor system
are involved? In the case of dementia, which domains of memory
are affected e just short-term or longer-term as well?
Patterns of central nervous system involvement
Different patterns of symptoms are produced by disease
involving different areas of the central nervous system, and it is
A line chart showing a patient’s description of the events
surrounding their most recent loss of consciousness
Visualizing the pattern of an individual episode helps the clinician
distinguish this problem as a probable seizure disorder and
sets the scene for a more focused, organized history.
Before episode –
“ I was sitting
reading a book” Prodrome –
Any residual deficit?
“three hours later I felt
completely normal again”
“ I had a sense
of deja vu”
Loses consciousness
After – “felt drowsy and tired”
During the event – “my brother said my
arms and legs were moving wildly and
my eyes rolled up in their sockets”
Time
Deficit Figure 1
Occurrence and severity of episodes for a pa tient
with migraine headaches
Severity of migraine
12 months
ago
6 months
ago
Present
consultation
Figure 2
MEDICINE 40:8 404 2012 Published by Elsevier Ltd.

3. Each episode may completely resolve or leave the patient
with a baseline level of disability from which their next relapse
will occur. Establishing what the baseline level of function
was before the current relapse is an important part of the history
in such cases.
important to recognize symptoms and signs that may help in
localization.
Cortical
Cortical pathology may be suggested by:
epileptic seizures
disturbances of consciousness
cognitive and psychiatric symptoms (e.g. dementia)
organic psychoses
hemiparesis
hemisensory disturbance
visual field deficits (homonymous hemianopia).
Pathological processes that commonly affect the cortex include
vascular disease, tumour, abscess and trauma, as well as
atrophy/infection for the temporal lobe. Remember that vascular
pathologies may not obey anatomical, lobar boundaries but
rather have distinct distributions relating to the cerebral arteries.
The motor and sensory cortices obey somatotopic organization
and one may localize motor paralysis, for example, to a partic-ular
territory depending on the relative weakness of upper and
lower limbs.
Frontal lobes are responsible for planning and executive func-tion,
and patients with frontal lobe damage may appear dis-inhibited
or flippant. Simple questions such as ‘how tall do you
think I am?’ may detect deficits. Check their attention span by
asking them to recall a string of numbers. Be aware that patients
with significant frontal lobe damage may lack capacity and need
a formal assessment of their ability to consent to investigation
and treatment. A wide range of symptoms can suggest frontal
lobe dysfunction, including changes in personality, mood and
insight, and urinary incontinence.
Parietal lesions: cortical sensory deficits can be difficult to
identify. Central sensory deficits need to be distinguished from
more common peripheral abnormalities. Simple loss of function,
such as temperature or proprioception, suggests a lesion lower
down the chain from receptor to cortex. Disorders such as
agnosia (can you identify what you are holding if you close your
eyes?), apraxia (an inability to perform gestures and complex
motor skills) or inattention suggest a cortical pathology.
Temporal lobes: speech and language may be affected if the
dominant temporal lobe is involved. Memory, particularly episodic
memory, is commonly affected by temporal lobe pathology. The
hippocampus and the temporal lobe are needed to form new
memories and are exquisitely sensitive to anoxia. Seizures origi-nating
in the temporal lobemay be preceded by a sense of dejavu, or
a strange smell. The medial temporal lobe is commonly involved in
viral encephalitis and acute temporal lobe symptoms associated
with headache in young patients should suggest this diagnosis.
Occipital lobes: cortical pathology may sometimes cause visual
deficits. Because the macula is over-represented in the cortex, in
the event of occipital lobe pathology the patient may be left with
a black spot in the visual field (a scotoma) where the macula,
rich in photoreceptors, is located. Enquire whether symptoms are
bilateral and, in particular, if there is any history of trauma; after
sudden deceleration, contre-coup injury may damage both
occipital poles simultaneously.
Extrapyramidal
Syndromes that impair movement, such as Parkinson’s disease,
cause a slowing of movement characterized by stiffness and
difficulties with activity, such as turning over in bed or turning
round. Such hypokineticehypertonic syndromes are due to lesions
in the pallidum or substantia nigra. Extrapyramidal diseases may
also cause involuntary movements including tremor. Putamen and
caudate lesions lead to a hyperkinetic syndrome in which tone
tends to decrease. Within this group, choreoathetosis describes
rapid changes in movements, often with a writhing or dancing
Line graph of disability against time for
relapsing–remitting multiple sclerosis (MS)
Disability
Time
Figure 3
Alzheimer’s dementia typifies a progressive
neurological disease
There is an unrelenting decrease in cognitive ability over time,
measured by mini-mental test scores for example.
Treatments, as shown by the arrow, may alter the disease
course but will not reverse it.
Cognitive ability
Progression
without intervention
Time
Figure 4
SYMPTOMS AND SIGNS
MEDICINE 40:8 405 2012 Published by Elsevier Ltd.

4. SYMPTOMS AND SIGNS
quality. Ballismus, although rare, is a more brief, violent and less
smooth involuntary movement that suggests a localized pathology
in the subthalamic nucleus. The differential diagnosis includes
genetic disease and degenerative pathology (see below).
Spinal cord
The spinal cord is symmetrically arranged into ascending and
descending columns, which are somatotopically organized.
Evaluation of a possible spinal cord lesion involves assessment of
the level(s) involved, whether the whole cross-section of the cord
is affected, and whether the pathology is intrinsic or extrinsic to
the cord.
A high transection of the cord in the cervical spine (due to
trauma) may result in spastic paralysis of all four limbs (tetra-plegia),
whereas the same pathology in the thoracic or lumbar
spine would affect just the lower limbs (paraplegia). In trying to
establish the level of spinal pathology, sensory symptoms are
also useful indicators, and a ‘sensory level’ should be sought on
examination. Involvement of the perineum with or without
associated autonomic dysfunction (such as urinary retention)
may indicate pathology in the conus or cauda equina.
Having established the level of the lesion, the distribution of
disease within the spinal cord should be assessed. Unilateral
symptoms as in the Brown-Sequard syndrome have a limited
number of causes, for example trauma, vascular insult and
tumour compression. Likewise, if there is an anterior cord
infarction due to spinal artery occlusion, symptoms may spare
the posterior cord columns (subserving touch, vibration and
proprioception). An expanding syrinx presses on central columns
but not peripheral ones, causing a cape-like sensory disturbance
and upper but not lower limb weakness.
Finally, consider whether the pathological process is from
within the spine or from outside it. Extrinsic compression may be
suggested by neck or back pain, malignancy which might have
metastasized to vertebrae, and recent procedures, such as epidural
anaesthesia or facet injection, possibly causing a haematoma or
abscess. With regard to intrinsic disease, the myelinated dorsal and
lateral columns are characteristically affected by dietary deficit of
vitamin B12 so one should ask if the patient eats well e ‘what is
a typical meal for you?’ e and whether they take excess alcohol. Is
there a history of syphilis? Untreated, this may lead to dorsal
column degeneration and a high stepping gait as the patient has no
proprioceptive feedback.
Root
A basic understanding of a dermatomal distribution of sensation
and muscle innervation is required. Root disturbance usually
causes pain that radiates into the muscles innervated by that
particular nerve root. For instance, in a C5 radiculopathy, the pain
radiates into C5-innervated muscles in the arm, causing weakness
of the deltoid and the other muscles innervated by C5, as well as
sensory disturbance in the C5 dermatomal distribution. The cau-ses
include disc herniation, herpes zoster, or tumours of the nerve
root. Metastasis can sometimes cause a focal radiculopathy.
Peripheral nerve lesions: give rise to weakness, wasting and
sensory disturbances. The latter may cause either positive symp-toms,
such as tingling and dysaesthesiae, or negative symptoms,
such as numbness or lack of sensation. Symmetrical peripheral
polyneuropathy usually affects the feet more than the hands
because these nerves are longer. The rate of onset of symptoms is
important to determine aetiology. For example, in GuillaineBarre
syndrome there is a rapid onset of symptoms over 1e4 weeks,
whereas in diabetic peripheral neuropathy the onset is slowly
progressive. (See later for useful questions.)
Myopathy
Muscle disease is a purely motor condition (without sensory
symptoms), as is motor neurone disease. Proximal myopathy
commonly presents with difficulty climbing stairs, rising from
a low chair or reaching up for things on a high shelf. It is
important to enquire about drug history as corticosteroids or
statins may be implicated. Pain and tenderness of the muscles
may suggest an inflammatory myopathy. Myasthenia gravis
causes fatigability with increased weakness after activity or later
in the day. Muscle disease may also have a genetic origin, so
a family history should be taken.
Further aspects to complete the history
Personal history
A patient’s educational background, personal development and
IQ may help in assessing the significance of cognitive symptoms.
Birth history may be relevant in patients with epilepsy or long-standing
neurological deficits. If infection is suspected, possible
exposure including recent foreign travel should be addressed.
Alcohol is an important neurological toxin and a realistic esti-mate
of use should be obtained.
Past medical history
Neurological involvement may occur in systemic conditions,
such as sarcoidosis, tuberculosis, or malignancy, so a general
medical history is important. A history of trauma to the head or
spine may also be relevant. Does the patient have ischaemic
heart disease, suggesting a risk of stroke? Ask when they last had
a brain scan, if ever. HIV status should be sought regardless of
gender or sexual orientation.
Drug history
A complete list of medications is essential because a number of
commonly prescribed medications (and vitamins) have neuro-logical
side effects. Peripheral neuropathy is a particularly
common problem and Box 1 lists some of the possible agents.
Ask when each medication was initiated, because adverse effects
(for example, parkinsonism as a result of atypical antipsychotics)
may be related to the extent of use. Substances of abuse are
always significant and in the case of intravenous drug use this
may be due to a direct pharmacological effect or infection.
Certain drugs (e.g. clozapine, bupropion) may lower the seizure
threshold in patients with epilepsy, while drug interactions may
cause acute toxicity (e.g. carbamazepine toxicity when erythro-mycin
is co-prescribed).9
Systems enquiry
Psychological e depression may result from or cause
neurological symptoms, so its presence should be sought.
The patient may not volunteer that they are depressed but
complain of feeling ‘down’, sad, tearful or ‘low’.
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5. SYMPTOMS AND SIGNS
Autonomic nervous system e are bladder, bowel and
sexual function normal? Does the patient complain of
lightheadedness or falls on standing? Autonomic
disturbance along with parkinsonism, for example,
may suggest multiple system atrophy as the diagnosis.10
Infections e does the patient have features of sepsis, such
as low-grade fever? Is there a history of recent infection?
Sore throat, myocarditis or diarrhoeal illness might point
to a post-infectious phenomenon, such as Sydenham’s
chorea or GuillaineBarre syndrome.
Rash or joint problems may indicate a vasculitis.
Cardiac symptoms are important when diagnosing the
cause of, loss of consciousness.
Sleep disturbance may indicate a brainstem lesion.
Features suggestive of malignancy (e.g. weight loss, poor
appetite, cough) should be enquired after.
A useful closing question is to ask whether the individual
thinks they have any other symptoms that may be relevant.
Family history
Some neurological disorders are inherited and a clear family tree
should be constructed, paying particular attention to the age of
onset of any neurological conditions, and family members who
have died young.
Social history
It is important to assess the individual’s home, work and other
activities to understand how their neurological symptoms affect
their ability to care for themselves in terms of walking, shopping,
dressing and bathing. An appreciation of their typical daily
routine and expectation of outcomes is helpful. This information
helps to determine decisions about management, as treatment
choice for many common chronic diseases depends on quality of
life and its alteration by the disease process.
Neurological system enquiry (Box 2)
It may be useful to develop a panel of questions to help identify
specific neurological symptoms or problems, particularly in
terms of their effect on everyday experiences. Examples include
whether there has been any change in the handwriting of
someone with a suspected extrapyramidal syndrome (which may
cause the writing to become smaller), whether the patient can
turn over in bed with ease, and whether they can keep up with
their peers when walking. They may also notice difficulty
walking through doors or initiating movement, indicating the
motor dysfunction associated with parkinsonism. Disturbances
of cognitive, autonomic and mood impairment should also be
explored in these patients.
Many junior neurologists fail to explore neurological symptoms
in sufficient detail. For example, they may fail to take note of the
typical aura that gives the clue to a diagnosis of migraine. The
patientmay need time to tell their story as well as prompts to allow
them to give a more detailed account. Sensory symptoms are
common and often not indicative of a serious neurological problem
(although numbness of the chin should be treated seriously as it
may indicate malignancy). Screening questions for sensory distur-bance
might include whether the patient can feel the texture of the
carpet or coldness of the tileswhen theywalk barefoot, andwhether
they can perceive hot or cold in the bath or shower. A
REFERENCES
1 Knecht S, Dr€age B, Deppe M, et al. Handedness and hemispheric
language dominance in healthy humans. Brain 2000; 123: 2512e8.
2 Hoefnagels WAJ, Padberg GW, Overweg J, Velde EA, Roos RAC.
Transient loss of consciousness: the value of the history for dis-tinguishing
seizure from syncope. J Neurol 1991; 238: 39e43.
Commonly prescribed drugs that may cause
peripheral neuropathy as an adverse effect
C Amiodarone
C Amitriptyline
C Dapsone
C Disulfiram
C Gold
C Hydralazine
C Isoniazid
C Lithium
C Metronidazole
C Nitrofurantoin
C Phenytoin
C Pyridoxine
C Reverse transcriptase inhibitors (as part of antiretroviral
therapy)
C Thalidomide
C Vinblastine
C Vincristine
(More detailed information may be found in the British National
Formulary.)
Box 1
Schema for neurological systems review
C Headaches
C Blackouts and loss of consciousness
C Cognitive function/mood
C Visual e eyesight, double vision
C Face
C Hearing
C Vertigo
C Speech
C Swallowing
C Arms e motor/sensory/pain
C Legs e motor/sensory/pain
C Balance
C Coordination
C Bladder
C Walking
C Neck and back pain
Box 2
MEDICINE 40:8 407 2012 Published by Elsevier Ltd.

6. SYMPTOMS AND SIGNS
3 Herzog AG. Catamenial epilepsy: definition, prevalence pathophysi-ology
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4 MacGregor EA, Hackshaw A. Prevalence of migraine on each day of
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simple index of independence useful in scoring improvement in the
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7 McDonald WI, Compston A, Edan G, et al. Recommended diagnostic
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8 Loveman E, Green C, Kirby J, et al. The clinical and cost-effectiveness
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9 Koppel BS. Contribution of drugs and drug interactions (prescribed,
over the counter, and illicit) to seizures and epilepsy. In: Ettinger AB,
Devinsky O, eds. Managing epilepsy and co-existing disorders.
Boston: Butterworth-Heinemann, 2002.
10 Quinn NP. How to diagnose multiple system atrophy. Mov Disord
2005; 20(suppl 12): S5e10.
FURTHER READING
Mumenthaler M, Appenzeller O. Neurologic differential diagnosis. 2nd
edn. New York: Thieme, 1992.
Patten J. Neurological differential diagnosis. 2nd edn. New York: Springer-
Verlag, 1998.
Swash M, Oxbury J, eds. Clinical neurology, vols. 1 and 2. Edinburgh:
Churchill Livingstone, 1991.
Wilkinson IMS. Essential
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