Central Nervous System
Symptomatology
Dr. Rasika Dharmadhikari
Department of
Practice Of Medicine
1. Syncope
The term ‘syncope’ refers to sudden loss
of consciousness due to reduced cerebral
perfusion.
‘Presyncope’ refers to light headedness
where the individual thinks he or she may
black out.
Syncope affects around 20% of the population
at some time and accounts for more than 5% of
hospital admissions.
Dizziness and presyncope are very common in
old age.
Symptoms are disabling, undermine confidence
and independence, and can affect an individual’s
ability to work or to drive.
There are several mechanisms that underlie
recurrent presyncope or syncope:
• Cardiac syncope due to mechanical cardiac
dysfunction or arrhythmia.
• Neurocardiogenic syncope in which an abnormal
autonomic reflex causes bradycardia and/or
hypotension.
Blackouts can also be caused by non-cardiac
pathology such as epilepsy, cerebrovascular
ischaemia or hypoglycaemia.
Differential diagnosis-
History-taking, from the patient or a witness, is the key
to establishing a diagnosis.
Attention should be given to potential triggers (e.g.
medication, exertion, posture), the victim’s appearance
(e.g. colour, seizure activity), the duration of the episode
and the speed of recovery.
Cardiac syncope is usually sudden but can be
associated with premonitory lightheadedness,
palpitation or chest discomfort.
The blackout is usually brief and recovery rapid.
Neurocardiogenic syncope will often be associated
with a situational trigger, and the patient may
experience flushing, nausea and malaise for
several minutes afterwards.
Patients with seizures do not exhibit pallor, may
have abnormal movements, usually take more than
5 minutes to recover and are often confused.
A history of rotational vertigo is suggestive of
a labyrinthine or vestibular disorder.
The pattern and description of the patient’s
symptoms should indicate the probable mechanism
and help to determine
subsequent investigations.
Neurocardiogenic syncope-
This encompasses a family of syndromes in which
bradycardia and/or hypotension occur because of a series
of abnormal autonomic reflexes. The two main conditions
are hypersensitive carotid sinus syndrome (HCSS)
and malignant vasovagal syncope.
Situational syncope-
This is the collective name given to some
variants of neurocardiogenic syncope that
occur in the presence of identifiable triggers
(e.g. cough syncope, micturition syncope).
Vasovagal syncope
This is normally triggered by a reduction in venous
return due to prolonged standing, excessive heat or a
large meal. It is mediated by the Bezold–Jarisch reflex,
in which there is an initial sympathetic activation that
leads to vigorous contraction of the relatively underfilled ventricles. This stimulates
ventricular mechanoreceptors, producing parasympathetic (vagal) activation
and sympathetic withdrawal, and causing bradycardia, vasodilatation or both. Head-up tilt-
table testing is a provocation test used to establish the diagnosis, and
involves asking the patient to lie on a table that is then
tilted to an angle of 60–70° for up to 45 minutes, while
the ECG and BP are monitored. A positive test is characterised by bradycardia (cardio-
inhibitory response) and/ or hypotension (vasodepressor response) associated
with typical symptoms. Initial management involves lifestyle modification (salt
supplementation and avoiding prolonged standing, dehydration or missing meals).
In resistant cases, drug therapy can be used; fludrocortisone, which causes sodium and
water retention and expands plasma volume, β-blockers, which inhibit the
initial sympathetic activation, disopyramide (a vagolytic agent) or midodrine (a
vasoconstrictor α-adrenoceptor agonist) may be helpful. A dual-chamber pacemaker can
be useful if symptoms are predominantly due to bradycardia. Patients with a urinary
sodium excretion of less than 170 mmol/day may respond to salt loading.
Carotid sinus hypersensitivity
This causes presyncope or syncope because of reflex
bradycardia and vasodilatation. Carotid baroreceptors are
involved in BP regulation and are activated by increased BP,
resulting in a vagal discharge that causes a compensatory
drop in BP. In HCSS the baroreceptor is sensitive to external pressure (e.g. during neck
movement or if a tight collar is worn), so that pressure over the carotid artery causes
an inappropriate and intense vagal discharge. The diagnosis can be established by
monitoring the ECG and BP during carotid sinus massage for 6 seconds. This manœuvre
should not be attempted in patients with a carotid bruit or
with a history of cerebrovascular disease because of the risk
of embolic stroke. A positive cardio-inhibitory response is
defined as a sinus pause of 3 seconds or more; a positive
vasodepressor response is defined as a fall in systolic BP of
more than 50mmHg. Carotid sinus pressure will produce
positive findings in about 10% of elderly individuals but
less than 25% of these experience spontaneous syncope.
Symptoms should not therefore be attributed to HCSS
unless they are reproduced by carotid sinus pressure. Dualchamber pacing usually prevents
syncope in patients with
the more common cardio-inhibitory response.
Postural hypotension
This is caused by a failure of the normal
compensatory
mechanisms. Relative hypovolaemia (often due
to excessive diuretic therapy), sympathetic
degeneration (diabetes mellitus, Parkinson’s
disease, ageing) and drug
therapy (vasodilators, antidepressants) can all
cause or
aggravate the problem. Treatment is often
ineffective;
however, withdrawing unnecessary medication
and
advising the patient to wear graduated elastic
stockings and get up slowly may be helpful.
Fludrocortisone,
which can expand blood volume through
sodium and
water retention, may be of value.
2. Vertigo & Dizziness-
Definition- Vertigo is defined as an abnormal
perception of movement of the environment
and occurs because of anabnormality in
sensory information from the eyes, limb
proprioception and the vestibular system
about a person’s position in space.
Vertigo commonly arises from inappropriate
input from the labyrinthine apparatus and
is within the experience of most people,
since this is the ‘dizziness’ which occurs after
someone has spun round vigorously and
then stops.
Benign paroxysmal positional vertigo-
This is due to the presence of otolithic
debris from the saccule or utricle affecting
the free flow of endolymph in the
semicircular canals (cupulolithiasis).
It may follow head injury, but is more
common in older patients who complain of
paroxysms of vertigo occurring with certain
head movements, typically looking up or
turning over in bed.
Each attack of vertigo lasts seconds but
patients often become very distressed and
reluctant to move their head, and this can
produce a muscle tension-type headache.
Secondary hyperventilation attacks and
associated depressive features are also
common.
BPPV Is Caused By Loose Calcium Crystals That Move Into One Of
The Small Tubes In The Inner Ear, Disrupting Normal Balance
Signals. The Effects Of This Disruption Can Be Felt As Vertigo Or A
Spinning Sensation When Moving Into Certain Positions.
Vertigo caused by labyrinthine disorders is
usually short-lived, though it may
recur, whilst vertigo arising from central
(brain-stem) disorders is often persistent and
accompanied by other signs of brain-stem
dysfunction. A careful analysis of the
history will reveal the likely cause in most
patients.
Treatment comprises explanation, along with
vestibular exercises designed to send the
otolithic debris back from semicircular canal
to saccule or utricle (such as the Epley
manœuvre) and/or to re-educate the brain to
cope with the inappropriate signals from the
labyrinth (such as Cawthorne–Cooksey
exercises).
The Epley manœuvre
It starts with the patient sitting upright on an
examination couch. They are asked to lie back with
their head turned at a 45˚ angle to the affected
side, and to hold this position
for 30–60 seconds. They should then be asked to
turn their head 90˚ to the opposite side and
remain in that position for 30–60 seconds. Next,
they should be asked to roll on to their side in the
direction they are facing, so that their face is
pointing towards the floor, and hold that position
for 30–60 seconds before sitting up once again.
Cawthorne Cooksey exercises involve asking
the patient to perform a series of eye, head
and whole-body movements whilst lying
down, sitting and standing.
Antihistamines can be tried if the condition
fails to respond to the above measures.
3. Fatigue-
Fatigue is a feeling of constant exhaustion,
burnout or lack of energy.
It can be physical, mental or a combination
of both.
Fatigue often occurs along with other
symptoms, such as:
- Depression and lack of desire to do the
activities you once enjoyed.
- Trouble concentrating or focusing.
- Very low energy and motivation.
- Nervousness, anxiety and irritability.
- Muscle pain and weakness.
Other fatigue symptoms include:
- Tired eyes
- Tired legs
- Whole body tiredness
- Stiff shoulders
- Malaise (discomfort/uneasiness)
- Boredom
- Impatience
Many conditions, disorders, medications and
lifestyle factors can cause fatigue. Fatigue can
be temporary, or it can be a chronic condition
(lasting six months or more).
Lifestyle habits-
- Poor diet
- Excessive alcohol use
- Illegal drug use.
- Stress
- Burnout
- Inactive (sedentary) lifestyle.
- Jet lag
Sleep disorders-
- Insomnia
- Sleep apnea
- Narcolepsy
- Shift work sleep disorder
Prescription medications and treatments-
Benzodiazepines, Sedative-hypnotics, Antipsychotics
Anxiolytics, Opioids, Anticonvulsants & Beta-
blockers
Infections-
Mononucleosis, HIV, COVID-19, Influenza
Pneumonia. Lyme disease.
Heart and lung problems-
Heart disease
Postural orthostatic tachycardia syndrome
(POTS)
Chronic obstructive pulmonary disease
Emphysema
Congestive heart failure
Mental health conditions-
Depression, Anxiety & PTSD
Autoimmune disorders-
Type 1 diabetes, Lupus, Multiple sclerosis
(MS), Myasthenia gravis, Rheumatoid
arthritis, Sjögren’s syndrome
Hormonal imbalances-
Problems with your endocrine system (the
glands in your body that make hormones) can
lead to exhaustion. Hypothyroidism is a
common cause of fatigue.
Other chronic conditions-
Cancer
Chronic fatigue syndrome
Fibromyalgia
Kidney disease
Type 2 diabetes
Weight issues and eating disorders-
Anorexia
Bulimia
Overweight/obesity
Underweight.
4. Neurological causes of weakness &
Paralysis-
Establishing the diagnosis in a patient with
weakness requires the application of basic
anatomy, physiology and some pathology to
the interpretation of the history and clinical
findings.
Weakness in only some muscles in a limb
suggests a problem in the peripheral nerve(s)
or motor root(s).
Weakness of the whole of one limb may be
due to problems in the brachial or
lumbosacral plexus, or to a central lesion.
Weakness in both lower limbs (paraparesis)
or in all four limbs (tetraparesis) suggests
either a spinal cord lesion or a diffuse
peripheral nerve problem such as Guillain–
Barré syndrome. In such cases the condition
of the reflexes is the most discriminating
sign.
The reflexes are absent in the Guillain–Barré
syndrome (or other lower motor nerve
lesions) and brisk in spinal cord (upper motor
neuron) lesions. The paraparesis or
tetraparesis of spinal cord lesions may be
associated with a specific pattern of sensory
loss which gives a clue to the site of the cord
lesion.
Patients with a bradykinetic limb often
complain of weakness. Therefore if there are
no reflex, wasting or sensory changes when a
patient is complaining of weakness in a limb,
extrapyramidal signs of rigidity (cogwheel or
leadpipe) and bradykinesia should be sought.
Patients with Parkinson’s disease usually
present with symptoms in one limb that may
be described as weak and clumsy, especially
for fine manipulations. Often the typical rest
tremor is a clue to the diagnosis
Weakness down one side of the body
(hemiparesis) is almost always due to a cerebral
hemisphere lesion, although it can be caused by
spinal cord or brain-stem lesions. The lesion is of
upper motor neuron type, and the site and often
the size of the lesion can be deduced by the
coexistence of other signs and symptoms, such
as higher cerebral function abnormalities or
sensory change. The evolution of a motor deficit
over time can give a clue to the underlying
pathology.
Alternatively, if a ‘weak’ limb is held up and then
suddenly allowed to drop, the limb may be
momentarily held up, something which does not
happen in organic weakness. Sometimes ‘non-
organic’ weakness may occur in combination with
weakness due to a neurological disorder and physical
signs such as ‘give-way weakness’ therefore do not
necessarily imply absence of pathology. Great care
should therefore be exercised in making the diagnosis
of functional weakness and all unusual
manifestations of nervous system disease should be
considered before such a
diagnosis is made.
Neurological causes
of weakness &
Paralysis
1. Weakness in only some muscles in a limb suggests
a problem in the peripheral nerve(s) or motor root(s).
2. Weakness of the whole of one limb may be due to
problems in the brachial or lumbosacral plexus, or to a
central lesion.
3. Weakness in both lower limbs (paraparesis)
or in all four limbs (tetraparesis) suggests either a spinal
cord lesion or a diffuse peripheral nerve problem such
as Guillain–Barré syndrome.
4. In such cases the condition of the reflexes is the most
discriminating sign.
5. The reflexes are absent in the Guillain–
Barré syndrome (or other lower motor
nerve lesions) and brisk in spinal cord
(upper motor neuron) lesions.
6. The paraparesis or tetraparesis of spinal
cord lesions may be associated
with a specific pattern of sensory loss
which gives a clue to the site of the cord
lesion.
Patients with a bradykinetic limb often complain
of weakness. Therefore if there are no reflex,
wasting or sensory changes when a patient is
complaining of weakness in a limb, extrapyramidal
signs of rigidity (cogwheel or leadpipe) and
bradykinesia should be sought.
Patients with Parkinson’s disease usually present
with symptoms in one limb that may be described
as weak and clumsy, especially for fine
manipulations. Often the typical rest tremor is a
clue to the diagnosis.
Weakness down one side of the body (hemiparesis)
is almost always due to a cerebral hemisphere lesion,
although it can be caused by spinal cord or brain-stem
lesions.
The lesion is of upper motor neuron type, and
the site and often the size of the lesion can be deduced
by the coexistence of other signs and symptoms, such
as higher cerebral function abnormalities or sensory
change. The evolution of a motor deficit over time can
give a clue to the underlying pathology.
Some patients may present with weakness which
is not due to organic disease but which is caused by
psychiatric illness such as a conversion disorder.
This type of weakness does not conform to known
patho-physiological patterns and the deficit cannot
be attributed to a lesion in a specific anatomical
site in the nervous system.
Gait disorders,
imbalance
& Falls
1. Pyramidal gait-
Upper motor neuron lesions cause a so-called pyramidal
gait in which the upper limb is held in flexion while the
ankle joint in the lower limb is kept relatively extended.
This causes a tendency for the toes to strike the ground
while walking and in an attempt to overcome this,
the leg is swung outwards at the hip (circumduction).
Nevertheless, the affected foot still scuffs along the
ground and the shoe on the affected side may be worn
at the toes as evidence of this type of gait. In hemiplegia,
the asymmetry between the affected and normal sides is
obvious in walking, but in paraparesis both lower limbs
swing slowly from the hips in extension and are dragged
stiffly over the ground. This can often be heard as well
as seen.
