Week 3 Central Nervous System
Learning outcomes
1 Anatomy,physiology of cerebral cortex,brain stem,cranial
nerves,Spinal cord and peripheral nervous system.
2.Student must have knowledge of ascending and descending pathways;
and clinical problems associated with lesion of these pathways.
3 Students must be able to localise site of CNS lesions
1 Cerebrovascular disease : elderly/young patient
2 Brain stem lesions – midbrain,pons,medulla
2.Cranial nerves : 3rd nerve’ , facial nerve
3. Spinal cord disease
4 Cerebellar lesions
4 Peripheral nerve lesions
5 Meningitis/encephalitis
6 Headache
Problem 1
A 60 year old patient presents with sudden onset of left sided weakness
and slurring of speech. (
)
dysarthria
Q.Take a relevant history from this patient.
-
orthopnea
-
PND
*
endogan
● Left-sided weakness:
○ Onset: sudden/insidious
○ Duration
○ Site: upper limb/lower limb/both
○ Affected limbs are spastic or flaccid
○ Associated symptoms: headache, nausea & vomiting, blurring
gxqflseeaxed
'
of vision, facial asymmetry/dribbling of saliva, sensory loss,
vision defects (reduced acuity/visual field)
○ Progression: rapid or slow
○ Ability to walk, carry out normal routines
● Slurring of speech: upper motor neuron facial nerve palsy
○ Onset, duration
○ Expressive dysphasia/receptive dysphasia/dysarthria
○ Associated symptoms: dysphagia, choking
● H/o balance problems, loss of consciousness
● H/o fever, trauma
● Past history: DM, HTN, dyslipidaemia, hypercholesterolaemia,
prosthetic valves, arrhythmia, previous same episodes, previous
h/o MI, stroke, any medication (aspirin/warfarin)
● Personal history/risk factors: smoking, alcohol, obesity
● Family history: DM, HTN, hyperlipidaemia, MI, stroke
-
.
{
● Handedness: dominant hand etc
Previous hx
-Lower limb: Ant cerebral artery lesion
-Upper limb: middle cerebral artery lesion
* Differential diagnoses:
•
social
↳ how the pro
recovered
↳ medication
history
Expressive dysphasia is a difficulty in expressing what you want to say. This may be in the form of speech but may also
affect their writing and reading aloud abilities. Speech may be non-fluent, and a person may find it difficult to find the
right word for something.
Receptive dysphasia is when a patient has difficulty with the understanding of written or spoken language. Patients
can both hear and see the words but not process and make sense of them.
Dysarthria is a motor speech disorder in which the muscles that are used to produce speech are damaged, paralyzed,
or weakened. The person with dysarthria cannot control their tongue or voice box and may slur words. There are
strategies to improve communication.
µ expressive aphasia
motor aphasia
cannot
↳
patient
express himself
sensory aphasia CReceptive)
↳ pro cannot express
-
homsaf
Dysphonia
↳ pt cannot
-
talk
loudly
↳ vocal cord problem
globus aphasia
-
cannottalk
cannot
Q.State the expected examination findings.
General examination
● Level of consciousness: GCS score
● Pulse : irregular rhythm (atrial fibrillation)
● BP: high
● Face: facial asymmetry, dribbling of saliva on left side
● Eyes: homonymous hemianopia (optic radiation involvement)
● CVS: Carotid bruit, JVP, murmurs (source of embolism)
● RS: signs of pulmonary oedema or infections
● Leg: pain and swelling (usually unilateral in DVT)
● Gait: hemiparetic gait hemiplegia gait
CNS examination
● Higher mental functions:
express
-
Judgement
○ Consciousness: alert and conscious, GCS score (14/15)
○ Orientation: well oriented (time place person) Ahistorical event
○ Memory: immediate, recent and remote memories are intact
○ Intelligence: intact Count / simple maths)
○ Speech: dysphasia/dysarthria
,
.
,
● Cranial nerve: do facial nerve , glossopharyngeal nerve
[
(swallowing problems)
]
● Motor:
○ Trophic changes: loss of hair, brittle nails, cold, shiny & dry
limbs
○ Unilateral (left) weakness (hemiparesis)/hemiplegia
○ Hypertonia of muscles (UMNL)
The Hoffman sign is an
involuntary flexion
○ Decreased muscle power of affected limbs
movement of the thumb
and or index finger when
○ Muscle wasting – no since it’s a UMNL , wasting common in
the examiner flicks the
fingernail of the middle
LMNL
finger down. The reflexive
Hemiparesis is a mild or
pathway causes the thumb ○ Pronator drift (left)
partial weakness or loss of
to flex and adduct quickly.
strength on one side of the
○
Tendon
reflexes:
hyperreflexia
(UMNL)
body. Hemiplegia is a
^
severe or complete loss of
○ Hoffman sign
strength or paralysis on one
side of the body.
● Sensory:
○ Unilateral (left) hemiparaesthesia/anaesthesia
○ E.g. : touch, pain, vibration, temperature
○ Loss of proprioception
○ Babinski’s sign: +ve on left side (UMNL)
● Optic nerve exam: visual field- homonymous hemianopia (since
optic radiation is affected)
● Check ankle clonus
is a rhythmic, oscillating, stretch reflex, the cause of which is not totally
> Clonus
known; however, it relates to lesions in upper motor neurons and therefore is
generally accompanied by hyperreflexia.
● Gait : hemiparotic gait- hip, knee, ankle extended, upperlimb
flexed, circumduction
CVS and RS exam:
cannot swallow
p patient
(aspiration pneumonia)g
- RS: crackle in right side of lung (since right bronchus is straight)
- CVS: carotid bruit in carotid artery in neck both sides, atrial
fibrillation, murmurs , BP
Q. State the investigations that you would do.
● CT scan of head- confirm site of lesion, extent of brain affected
● FBC - exclude anemia, polycythemia, thrombocytosis
● Blood sugar - exclude hypoglycemia/DM
● Blood urea and serum creatinine - to know hydration status
● Serum lipid profile
↳ to rule out renal failure
● Serum electrolyte
● Chest X Ray → cardiomegaly
● ECG → to rule out arrhythmias , hypertrophy I left ventricular) , mi
● Echocardiography in suspected cardioembolism: C
Atrial fibrillation – atria
cannot contract properly , so thrombus formation in atrium,, left ventricular
hypertrophy
● Carotid duplex Ultrasound to identify extracranial vessel disease
● Transcranial Doppler Ultrasound to identify intracranial vessel disease
● MR angiography (MRA) or CTA of cerebral vessel
CT scan of patient is shown:
F-
Rt
.
Ventricle
compressed
Q Describe the radiological findings.
● Hypodensity of right cerebral hemisphere – cerebral infarct (due to
ischemic stroke)
● Swelling and compression of right ventricle with midline shift to
the left
● Loss of grey white matter differentiation
● Massive right-sided cerebral infarction
Q State the likely diagnosis
Cerebrovascular Accident (ischaemic stroke) with left sided hemiplegia
Q. Mention the underlying pathogenesis of this clinical problem.
Ischemic stroke is due to sudden occlusion of an intracranial vessel with
reduction in blood flow to the brain area supplied by that vessel.
Occlusion happens either due to in situ thrombosis (atherosclerotic
vessel) or embolus from a distant site (internal carotid and aortic arch)
Three main causes of ischaemic stroke are:
● Atherothromboembolism (50%)
● Intracranial small vessel disease (penetrating artery disease) (25%)
● Cardiogenic embolism (20%)
plaque ruptures
→
Thrombi embolic
event
Other causes include arterial dissection, trauma, vasculitis
(primary/secondary), metabolic disorders, congenital disorders and other
less common causes such as migraine, pregnancy, oral contraceptives,
etc.
Acute occlusion of intracranial vessel > Reduce blood flow to the brain
region it supplies > Ischaemia/Infarction depend on severity of reduction
of blood flow. If blood is restored before significant amount of cell
death, patient may experience only transient symptoms (Transient
Ischaemic Attack). The infarcted area is surrounded by ischaemic areas
(ischaemic penumbra) where if blood flow is restored within reasonable
time, the changes are reversible. If blood flow is not restored, it will
eventually undergo infarction (irreversible cell death).
Biochemical changes: Hypoxia > Mitochondria cannot produce ATP >
Failure of membrane pump > Cytotoxic edema and membrane
depolarization > Calcium enter cell and glutamate is release from
synaptic terminals > Glutamate lead to intracellular calcium
accumulation > Excess calcium inside neurons produces free radical by
membrane degradation and mitochondrial dysfunction > Death of
neuronal cell
Q. Outline management.
Admit to multidisciplinary stroke unit
General measures:
1. Assess airway, breathing and circulation.
2. Ensure clear airway. Keep the patient nil by mouth.
3. Give oxygen by mask if low saturation.
4. Monitor BP and pulse. Do not treat HPT if SBP is < 220mmHg or
DBP < 120 mmHg. Mild HPT is desirable at 160-180/90-100
mmHg. BP reduction should not be drastic.
5. If dehydrated, give fluids parenterally.
6. Assess nutritional status. If dysphagia persists, feed via nasogastric
tube.
7. Monitor blood glucose. Treat hyperglycemia with insulin and
hypoglycemia with glucose infusion
8. If patient has fever, investigate and treat the causes. Give
antipyretics
9. Regular change of posture to avoid bed sores.
10. Care of bowel and bladder to avoid infection.
11. Control Hypertension/DM/Dyslipidemia.
12. If patient develops cerebral edema, give IV mannitol 0.25-0.5
g/kg and head end elevation.
13. If hydrocephalus is present, drainage of cerebrospinal fluid via an
intraventricular catheter
14. Hemicraniectomy and temporal lobe resection if infarction is very
large
Ateplase?
Specific treatment (Reperfusion):
¥
"
T
1. Intravenous Thrombolysis: Intravenous rt-PA (0.9mg/kg,
-
maximum 90mg), with 10% of the dose given as a bolus followed
by a 60-minute infusion, is recommended within 4 hours of onset
of ischaemic stroke.
IV rt-PA is given only if there is a physician that expertise to
manage stroke, availability of appropriate neuroimaging test, and
can manage complication of thrombolysis (intracranial
hemorrhage)
The main contraindications are bleeding risk (recent haemorrhage,
anticoagulant therapy), delay to treatment, high BP
>185/110mmHg, recent major surgery, prior stroke or head injury
within 3 months, GI bleeding in preceding 3 weeks
2. Antithrombotic treatment: Start aspirin within 48 hours of stroke
heparin
[
onset. Use of aspirin within 24 hours of rt-PA is not recommended.
If thrombolytic is contraindicated, give 300 mg/day of aspirin
3. Anticoagulant (Heparin and LMWH) not routinely recommended
4. Endovascular techniques: Intra-arterial thrombolysis and
endovascular thrombectomy
5. Rehabilitation: Early physical and speech therapy
embolic
or
isheemic
→ Thrombohsse
stroke?
thrombotic
→
aspirin
* embone stroke :
Long-term management:
↳ heparin
-
.
1. Address the RF (HPT, Smoking, Obese, DM, Alcohol)
2. Antiplatelet: Aspirin 75mg-325mg daily
3. Heparin is given if there is AF
4. Anti-HPT: ACE-inhibitor or ARB
5. Lipid reduction with simvastatin 40 mg
6. Control blood glucose level
7. Stop smoking and reduce alcohol intake
8. Carotid endarterectomy if internal carotid artery stenosis >70%
Discuss lobes in cortex and cerebral function of different cortical centres
Lobe
Normal Function
Frontal Lobe
Personality, Emotional response, Social behaviour
Parietal Lobe
Dominant side: Calculation, Language, Planned
movement, Stereognosis
Non-dominant side: Spatial orientation,
Constructional skills
Temporal Lobe Dominant side: Auditory Function, Speech,
Language, Verbal Memory, Olfaction
Non-dominant side: Auditory function, Music,
tone sequences, Non-verbal memory (music,
faces), Olfaction
Occipital Lobe Analysis of vision
*NOTES:
Types of stroke:
1. Ischaemic stroke (82%):
a. Thrombotic
b. Embolic
An ischemic stroke is when blood vessels to the brain become clogged. A hemorrhagic stroke is when bleeding
interferes with the brain's ability to function. A stroke is a medical condition where there is an interruption in
blood flow to the brain.
2. Haemorrhagic stroke (15%):
a. Intracerebral
b. Subarachnoid (rare:3%)
Risk factors:
1. Diabetes
2. Hypertension
3. Obesity: hyperlipidaemia
4. Smoking
5. Alcohol
Causes of stroke:
Old patient
Heart diseases
E.g.: Atrial fibrillation, valvular
disease, IHD
Hypertension, diabetes
Atherosclerosis
Trauma
Problem 2
Young patient
Infective endocarditis
Rheumatic heart disease
OCP intake
SLE: vasculitis
Atrial fibrillation, prosthetic
valves
Tuberculosis
Berry aneurysm
Trauma
Q.Interpret this CT scan
D) ✗
→
Hemorrhagic stroke on right hemisphere
-Bright white area – hyperdense area on the right hemisphere on frontal
area
-Midline shift to the left
-irregular margins
-cerebral edema – around the hemorrhage
Q.Mention the clinical presentation of these patients.
-Sudden onset of severe headache, vomitting, loss of consciousness
-Sudden onset left sided hemiplagia/hemiparesis
-May be associated with slurring of speech
-Mental confusion
Q.State the complications of stroke
-Epileptic seizures
-Recurrence of stroke
-Dvt/ pressure sores (immobile)
-Depression, anxiety
-Intracerebral hemorrhage
-Hydrocephalus
-Pulmonary embolism
- Aspiration Pneumonia
-UTI
-Cerebral edema
-Contractures (not exercising)
Q.Outline management.
-Surgical removal of hematoma if severe
-Nursing management (turn patient every 2 hours to prevent bed sores)
-Management of risk factors : ACE inhibitors, CCB, Beta blockers for
HTN, control glucose for DM
-
-No anticoagulants/antiplatelets
→
physiotherapy
causes
bleeding
- HTN and bradycardia (Cushings reflex), nausea vomiting, headache
(increased ICP) - cerebral edema à give IV mannitol
(end organ damage – hypertensive emergency)
f Gcs
→
unequal pupils
→
herniation
side
②ilatiof @
herniation)
on
brain
Q.Describe in brief anatomy and blood supply of cerebrum.
Ant & Medial Cerebral artery : Frontal and temporal lobe
Verterobasillar system : Occipital lobe, midbrain, cerebellum
Communicating arteries : Left and right hemispheres
Q.Describe Cushing’s reflex.
-Blood flow to the brain is directly related to cerebral perfusion pressure
(CPP)
-CPP = Mean Arterial Pressure(MAP) - Intracranial Pressure (ICP)
-Therefore MAP must be greater than ICP for perfusion of the brain
-When MAP is lesser than ICP the hypothalamus activates sympathetic
nervous system causing peripheral vasoconstriction and an increase in
cardiac output
-As a result of the increased arterial pressure, the baroreceptors in the
carotid bodies are stimulated slowing the heart rate down to bradycardia.
-Known as Cushings reflex/ CNS ischemic response/ Vasopressor
response
- Cushing Triad : Presence of HTN ( increase systolic, decreased
diastolic), Bradycardia and irregular respiration in patients with raised
ICP. Irregular respiration is due to reduced perfusion of brainstem or
possible brainstem herniation
after
cerebral
quelling
event
→
T
ICP
compress
)
vessel
Q.How would you grade a comatose patient?
→
t
perfusion
t
Sym
I
Uasocmt
:
6
Q.List the differences between Upper and Lower motor neuron lesions.
Q. Discuss lobes in cortex and cerebral function of different cortical
centres
Localisation of lesion
Problem 3
[
Q.A 70 year old patient presented with right sided weakness of 3days
duration.He was able to comprehend but able to speak only few words.
Where is the lesion? Explain with diagrams
Site - Left sided frontal lobe
atthe pre central gyrus
Global aphasia: Wernicke + Broca
.
-
(
(fluent comprehend repeat)
Wernicke’s aphasia: Sensory aphasia Yes (fluent) No
Comprehend repeat)
[Broca’s aphasia: Motor aphasia – expressive Yes Comprehend) No fflmnt
No
,
,
,
Find handedness: right or left side dominance
,
,
Problem 4
Q.A 50 year old patient presents with inability to frown on right side and
drooling of saliva on right. He also had left sided hemiparesis.
1. Where is the lesion? Explain
Right lower part of Pontine lesion
EXPLAIN: Mouth deviated to left side, Drooling of saliva on the
right,Drooping of eyelids onto right side and LMN facial paralysis
2. What is the difference between upper and lower motor neuron
,
repeat)
✗
✗
i.
~
upper
31
lower
damage
face
lower
damage
face
ñÉÉ
p¥÷
t
'
e
facial palsy.
i
Types of facial nerve palsy:
UMN facial nerve palsy and LMN facial nerve palsy
- If one whole half is affected: LMN nerve palsy – due to
whole facial nerve or nucleus lesion
- If lower half of face affected : UMN nerve palsy –
corticobulbar fibres affected
(upper half of face is supplied by both sides of corticobulbar fibres
lower half of face is only supplied by contralateral corticobulbar
fibres)
LMN – contralateral facial and hemiparesis
contralateral
UMN – ipsilateral facial and hemiparesis
Contralateral is defined as
'pertaining to the other side'.
Ipsilateral is considered the
opposite of contralateral and
occurs on the same side
3. What is Bell’s palsy?( Explain in detail the causes you need to
exclude)
Acute isolated facial nerve palsy could be due to viral infection or
idiopathic causing swelling of the nerve within the tight petrous bone
facial canal. (Treatment: short course of steroids. )
Diagnosis of exclusion – exclude pontine lesion, Ramsay hunt
syndrome, acoustic neuroma, otitis media, mastoiditis etc , then come to
conclusion that it is Bells Palsy
Presents with:
-
Unilateral LMN facial weakness
Loss or altered taste on the tongue
Pain behind the ear
Vague altered facial sensation
→
Facial nerve nucleus is in the pons
Niue
Causes: 1. Pontine lesion is determined by:
-
didnt
Contralateral hemiplegia (corticospinal tract)
6th and 7th nerve lesion. Ipsilateral LMNL facial nerve palsy
6th nerve palsy: lateral rectus, inability to abduct eye
discuss
2. Geniculate ganglion lesion:
-
Ramsay hunt syndrome : reactiviation of herpes zoster virus
Check for herpes zoster lesions in ear (external pinna), or
rarely in throat
hearing loss on affected side
4. Cerebellar Pontine Angle : known as acoustic neuroma
- 5th CN
µxo%Ñ
1. check for muscles of mastication ( masseter,
temporalis)
2. Hyper movement of lower jaw (jaw jerk)
-
- 8th CN :
>
r
1. Reiners and webbers test, – Reiners: BC>AC ,
Webers: lateralising to affected side
- Cerebellar lesion signs:
2. wide based gait, fall towards side of lesion,
nose
$
heel Shin
3. dysmetria, dysdiadokokinesia,
c4. scanning speech (dysarthria)
5. nystagmus
hearing
loss
n
1. rombergs sign,
finger /
conductive
t
muscle
speech
(slurring)
.
Weber's
€
pysmetria
4. Facial canal : otitis media, mastoditis – check for pus in the ear
-
nerve to chorda tympani: loss of taste to ant 2/3 of tongue
nerve to stapedius: can’t tolerate loud sounds
stylomastoid foramen :
-
parotid gland enlargement ( tumor)
Complications of Bells Palsy:
-
6
due to viral
→ isolated
:
*Treatment of Bells Patsy
↳ short courses of
t.MN lesion
steroid
.
- cant close eye and is exposed à keratitis, corneal ulcers,
infection.de
abrasion (close eye with eye patch throughout day, give
eye drops as eyes beocme dry, surgery – lateral side of
eye sew up eye become smaller
- Reinervation : unwanted facial movement, abarrant
innervation, while eating is tearing (tears at wrong
time- due to abnormal inervation of nerves)
5. Outline origin and course of 7th cranial nerve
①-
②③④⑤⑥-
⑦⑧⑨-
④①-
Nerve arises in the pons and begins as two roots: large motor
root and smaller sensory root.
Two roots enter internal acoustic meatus of temporal bone.
Enter facial canal
Two roots fuse to form facial nerve
Nerve forms geniculate ganglion
Nerve gives rise to: greater petrosal nerve, nerve to stapedius
, chorda tympani
Exits facial canal via stylomastoid foramen.
Facial nerve runs ant to outer ear
Gives rise to post auricular nerve
Continues into parotid gland
Terminates by splitting into : temporal branch, zygomatic
branch, buccal branch, marginal mandibular branch, cervical
branch
MMC
TZB
-
f
①
②
Int Acoustic
.
meatus
Fgf
④
temporal
facial
bone
canal
③
⑤
⑥
④
⑦
⑧
①
⑨
④
Problem 5
Q. A 40 year old hypertensive patient presents with sudden onset of
unsteady gait and a tendency to fall towards the right.
1. Where is the possible site of lesion?
Right cerebellum
2. What are the findings you would look for on examination of this
patient.
● Gait: tandem gait test (Heel-to-Toe) is abnormal
● Cerebellar ataxia : Patient falls over when bringing feet together
● Dysmetria: overshooting of fingers in finger nose test
● Intentional tremors
● Dysdiadochokinesia: finger-nose test (inability to perform rapid,
●
●
●
alternating movements)
Pendular knee jerk (swinging)
Nystagmus (involuntary, rapid and repetitive movement of the
eyes)
Scanning/ staccato speech pattern (pauses between words- British
parliament
● Rebound phenomenon
3. Discuss causes.
● Posterior circulation stroke
● Tumours in cerebellum hemengiobbst
● Spinocerebellar ataxia
● Multiple sclerosis
● Post herpes zoster infection
-
ma
,
meduwblastons
● Alcohol
● Drugs eg phenytoin, carbamazepine
-
● Wallenberg syndrome:
● Horners syndrome
● Contralateral spinothalamic lesion
4. Discuss anatomy and spinal tracts in brain stem.-midbrain,pons
and medulla
Midbrain
Nim
didnt
discuss
Right mid brain lesion :
- left sided hemiplegia
- right 3rd and 4th cranial nerve lesion
Pons
fascial nerve goes around the abducent nerve
if right side of pons affected: LMN lesion
- right facial palsy – fascial nerve affected
- 6th right nerve supplies lateral rectus – abduct and look to right then the
eye wont move due to abducent nerve lesion
- left hemiplegia – pyrimidal fibers havent decessated yet
Medulla
- Ipisilateral 9,10,11,12 nerve palsy
- Contralateral hemiplegia
Spinal tracts of brainstem:
Descending tract
● Pyramidal (voluntary)
- Ant and lateral corticospinal (voluntary motor control of body)
- Corticobulbar (voluntary motor control of head and neck)
● Extrapyramidal (involuntary motor control)
- Rubrospinal
- Reticulospinal
- Tectospinal
- vestibulospinal
Ascending Tract
● Posterior column (fine touch and proprioception)
● Anterior spinothalamic tract (crude touch and pressure)
● Lateral spinothalamic (pain and temperature) – crosses to opposite side
before ascending
● Ant and post spinocerebellar (unconscious proprioception)
● Spinoolivary (unconscious proprioception)
Problem 6
Q. 57 year old male presents with weakness of both lower limbs for 3
months. Weakness progressively increased and patient on admission was
unable to walk .Also had evening rise of temperature (suggests infection
– possible TB) .No trauma.Bladder and bowel habits were
normal.Patient was noted to have back pain around 10th thoracic
vertebra.
1. What further examination would you like to carry out.State
expected findings
●
​Spastic paraplegia
●
​Sacral loss of sensation
●
​Weakness of leg
●
​Babinski sign positive
port's disease
-
examination: UMNL
- no muscle wasting
- hypertonia
examine
.
- hyperreflexia
- babinski positive
- sensation: T10 compression (roughly around umbilicus so
below umbilicus all sensations lost)
2. What is the likely diagnosis.
● Spinal cord compression
3. State investigations you would like to carry out.
-MRI spine – show collapse of vertebra, decreased joint space
-biopsy- cold abscess
-for TB : mantoux test
→ or
myehgram
.
-X Ray spine
-Serum B12 - Subacute combined degeneration
Treatment:
-if compression present- decompress
-Anti TB regime – INH, Rifampicin, pyrazinamide, ethambutal for
arounf 1 year
4. Explain what is cauda equina and conus medullaris syndrome.
Cauda equina syndrome: cauda equina bundle of nerves damaged
Conus medullaris syndrome: damaged to the conus medullaris (or
terminalis), at the end of the spinal cord
Conus medularis : tapered lower end of spinal cord
• Presentation : sudden and bilateral
• Reflexes: diminished at the level, brisk below the level. (UMN)
• Radicular pain : (-) less
• Lower back pain: more, early
• Impotence : frequent
• Numbness: symmetrical
• Motor strength: symmetrical , hyper reflexic, distal paralysis of lower limbs .
• Sphincter dysfunction : present early both urinary and fecal inconsistence
• UMN
Cauda equina : bundle of nerves below the end of spinal cord
• Presentation : gradual and unilateral
• Reflexes: diminished because its peripheral nerve involvement
• Radicular pain : + more shooting pain (due to peripheral nerve involvement)
• Lower back pain: less
• Impotence : absent
• Numbness: Asymmetrical
• Motor strength: Asymmetrical , Areflexic , paraplegia
• Sphincter dysfunction : present later, only urinary retention
• LMN
Problem 7
Q. A 25 year old foreign worker is admitted with tingling and numbness
of both lower limbs..Subsequently,it spread to the upper limbs.
1. What is the likely diagnosis?
2. State the expected examination findings.
3. State how you would confirm your diagnosis.
4. Outline management.
List differential diagnosis of patients with peripheral neuropathies.
a.What is the likely diagnosis.
Guillain Barre syndrome- autoimmune (minimal sensory loss, generally
motor loss)
Hx:
- how it started , spread , duration
- preceeding infection
- starts in lower limbs and ascends upwards fast
LMN signs as peripheral nerves are involved
b.State the expected examination findings.
Sensory
●
​Distal paresthesia and pain in muscles
●
​More proximal part of the muscles
Motor
●
​Areflexic*** - suspect Guillain Barre
●
​Facial and Bulbar weakness
●
​Diffuse weakness and loss of reflex
µµHP0i
y
Respiratory weakness which can lead to respiratory failure
Miller-Fisher syndrome: Internal and external ophthalmoplegia, ataxia
and areflexia
c.State how you would confirm your diagnosis.
●
​CSF- Increase protein, WBC normal (Cytoalbuminemic
dissociation of CSF)
7
●
​Electrophysiological changes- conduction block, multifocal
motor slowing, delayed f waves
​Antibodies to ganglioside GM1
●
d. Outline management.
​Plasma exchange
●
IV.
immunoglobulin
●
​iv Ig therapy ; for 5 days at 0.4g/
●
​Nursing measures to prevent bed sores and DVT
●
​Monitor respiratory functions, intubate if needed (patient
recovers after 2-3 weeks usually)
I
t
90% patients recovers
→
Protein
↳
Lumbar
T
,
cell
Cytoalbumic
puncture
:
count
normal
disassociation
left lateral fetal position
and insert between 13,14
DDx for Guillain Barre: Hypokalemia, polio, botulinum, myasthenia gravis, cord
compression, transverse myelitis
DX
peripheral neuropathy
isoniazid alcoholism
→
,
,
myasthenia gravis
,
-
-
-
opthnnluwpluju
A reflex
Ataxia
Problem 8
Q.A 30 year old patient presents with fever of 5 days.He also has
headache,vomiting and appears drowsy.
1. What is the likely diagnosis?
Meningitis
2. Discuss the different etiological causes.
-
photophobia
,
sericeous
headache
-
Kerning
budzinski
,
vomit
,
ia
,
3. Mention the investigation you would do and expected results.
● CT Scan for contraindication of lumbar puncture
● Lumbar puncture for CSF (make sure no increased ICP symptoms
d-
– nausea, vomiting , headache, papilledema)
● Blood culture
● PCR
T
,
=fmdɢtw
↳
papiledema
-
→
wise
brain
herniated
blurred margins
tortuous
,
haemorrhage
,
vessels
* if
papiledemn
then
Lumber
Pune
contraindicated
4. Explain how analysis of CSF will help you determine the
etiological cause?
e. Hx taking
usual complaint: fever, headache drowsy, neck stiffness, altered
consciousness, rash(petechial, purpura), vomiting, photophobia, focal
neurological deficit.
Fever:
Onset and duration of fever?
When does is start ( morning, evening, night)
Progression (few hrs, all day, night only) + evening rise of temp + night
sweats?
Associating symptoms (night sweats, chills, rigor, rash, urinary
complain, cough, chest pain, pain abdomen, headache, loss of
consciousness, weight loss, polyarthritis)
Hx of sexual exposure, sex hx, travel history?
Medication taken?
Headache:
.
Site ?
Time of onset?
Severity?
Nature of headache? (throbbing, burning)
How does it start ?
How long does it persist?
Recurrent?
Aggravating factor ( coughing, straining, or change of posture) ?
Relieving factor?
Preceding by aura?
Associate fever vomit weakness blurring vision vertigo nasal stuffiness,
lacrimation, breathlessness?
Examination :
Complies
encephalitis
infee
spreed
if
Neck stiffness:
→
Kerning sign
Brudzinski sign – flex neck , knee and hip flexed
→
→
Treatment
IV penicillin
(N
.
meningitis)
3rd gen cephalosporin
co
-
14
days ]
herniation
brain
due
ICP
to
→ Vision
→
abscess
cerebral
31
hearing
septicemia
Problem 9
Q.A 42 year old patient presents with left sided headaches for last 6
months.He also says that headache is associated with nausea and
T
loss
vomiting.
He has 2 attacks per week and unable to work during the
headaches.Mother has similar problems.
grain
became
familial
1. What further history would you take?
2. Discuss the differential diagnosis of headaches.Explain with
reasons.
3. What characteristics of headaches warrant further investigations?
1)Further history to be taken:
● Site of headache pain: ( unilateral presents in migraine)
● Onset of headache : sudden/gradual
If headache is constant or come & go?
● Character of headache( if throbbing / band-like)
● Radiation present?
● Aggravating & Relieving factors of headache:
● If patient have history of any medication, substance abuse, head
trauma.
● Associated symptoms such as fever & neck stiffness, photophobia
● Triggering factors: Caffeine (migraine), stress,dehydration,
excessive codeine use
● Time: Did headache changed over time?
If it worsen in mornings or any particular time of the day?
● How often headache symptoms last each episode?
● Severity of headache : If headache affects daily functioning of life?
● Aura – preceding manifestation (warning sign) 80% don’t have
aura
same
y
time
several
for
days
1
morning
to
noon
highest
-
-
Rhinos sheer
lacrimation
2. DD
● Hereditary migraine ( without aura ) - not associated with sensory
disturbance
Unilateral suggestive of migraine headaches
Episodic in nature and not more than twice a week
Has familial predisposition of migraine from 1st-degree relative
● Tension-type headache - patient presents with primary headache
symptoms
No known underlying conditions or causes
To rule out co-existing mixed chronic daily headache
3. (i) - lateralized and severe head pain, followed by fixed neurological
deficit: arterial dissection is considered
- Unilateral pain localized to the face, frontal region or eye: carotid
dissection
- Unilateral or bilateral occipital pain: vertebral dissection
(ii) - Headache of raised intracranial pressure-type, like headache
worsens on walking, exacerbated by coughing, sneezing or straining:
feature of cerebral venous sinus thrombosis (in which focal signs
including seizures are found)
- Usual presentation: subacute raised pressure
(iii) - Sudden, severe headache: subarachnoid hemorrhage (most imp
symptom)
- Cardinal symptom: exceptionally rapid onset, described as being
‘like a hammer blow to the head’ or ‘explosion in the head’
- Reaches maximum in a split second: is termed as ‘Thunderclap
headache’
- Other symptoms: occipital localization of pain, neck stiffness,
nausea, vomiting, and exertion or Valsalva immediately preceding
to headache
- CT scan is done to seek evidence of acute subarachnoid blood, if CT
is (-) a lumbar puncture is done to look for red cells or their
breakdown product
(iv) - Aching, or throbbing headache exacerbated by coughing, bending
over or straining, worsens in the morning and causes wakening from
sleep, worsens on exertion or on lying flat
- As headache worsens vomiting,diplopia, and papilloedema develop
- Raised intracranial pressure(ICT): may due to obstruction of normal
CSF flow by an intracranial tumour or another mechanism
affecting CSF dynamics.
- First clinical priority: exclude an intracranial mass lesion by
imaging with CT or MRI
- If there is no mass lesion, can be due to other mechanisms:
-
(v) - Angle closure glaucoma(acute raised pressure in the eyeball) may
lead to headache, particularly around the eye, as well as visual
abnormalities, nausea, vomiting and a red eye with a dilated pupil.
(vi) Headache in older people, particularly when associated with visual
symptoms or jaw claudication, may indicate giant cell arteritis (GCA), in
which the blood vessel wall is inflamed and obstructs blood flow.
Management:
Sumitriptan (acute attack) ,
Prophylaxis: b blockers
What characteristics of headaches warrant further investigations?
-Stabbing headache, excruciating pain (subarachnoid hemorrhage)
-Thunderclap headache
-Examination: neck stiffness (suspect subarachnoid hemorrhage)
-headache, vomiting à investigation required
CT scan for subarachnoid haemorrhage
Red flag signs:
-Loss of consciousness
-Paralysis of a limb
-Neurological signs
-< 40 is more worrying
-Raise ICP
-Vomiting , fever
-Weight loss, raised BP
-Prolonged cough with headache