Nervous System
History and examination
Dr.Shailesh Kamble( MSc
Human Anatomy)
Overview
Aim
The session will also introduce the
special features of neurological history
taking and examination and the
language of neurology.
Learning outcomes
Describe the special features of the
neurological history and examination
Define some neurological terms
Neurons are the building blocks.
Astrocytes provide structural framework whereas microglial cells are concerned with immune
and scavenging functions.
CNS- oligodendrocytes produces myelin sheath
PNS- Schwann cells produce myelin sheath.
Volume of CSF is around 140-270 ml which is replenished 3 to 4 times in a day with
production rate of 700mL/day.
Spinal cord contains afferent and efferent pathways which are responsible for motor and
sensory information transmission.
Sensory cell bodies of peripheral nerves are in the dorsal root ganglion.
Motor cell bodies are located in the anterior horn of the spinal cord.
General introduction
History
TIME RELATIONSHIP
 For common neurological symptoms such as
headaches, numbness, loss of consciousness,
history is the key to diagnosis.
 ALWAYS THINK WHERE IS THE LESION? WHAT
IS THE LESION?
 Always remember to ask patients to define
symptoms in their own language.
O- onset(When did the symptom start?/when was he
well last time?)
(sudden, gradual/evolving)
D- duration(Persistent/intermittent)
P- progress ( Better or worse or same)
 What was the patient doing when the symptoms occurred?(Precipitating factor)
 Anything which makes the patient's symptoms better or worse( time of the day, menstrual
cycles, posture or medications)(Relieving/exacerbating factors
Precipitating, exacerbating or relieving factors
Associated
symptoms
 With every disease you have
associated symptoms like in
case of headache you will
have nausea, vomiting,
photophobia( aversion to
light) or
phonophobia( aversion to
sound)
Presenting complaint in neurology
Common
Headaches
Dizziness
Pain
Numbness
Pins and needles
Weakness
Others
Memory
Shaking
Vision
Confusion
Loss of
consciousness
Questions
• Describe it to me?
• Frequency?
• Location?
• Precipitant, exacerbating/alleviating factors?
• RED FLAGS
• Thunderclap headache
• Slurred speech, weakness
• Incontinence of bladder/bowels
• Bilateral sciatica
• Seizures
• Acute confusion
• Fever
• Non blanching rash
Other histories
 PAST MEDICAL HISTORY- Symptoms which patients usually forget, birth history or
development history( in epilepsy), or hypertension, diabetes.
 DRUG HISTORY- Prescribed, over the counters, complementary or recreational drugs.
 FAMILY HISTORY- First degree relatives
 SOCIAL HISTORY- Coping with the symptoms, affecting work?
Diet history especially vegetarians(VIT B12 intake), alcohol intake, drugs,
STDs, travel history
 OCCUPATIONAL HISTORY- toxic peripheral neuropathy due to exposure any metals,
epilepsy for driving, cognitive levels for dementia.
PHYSICAL EXAMINATION
 Physical examination begins
when the patient enters the
clinic. OBSERVE FACIAL
EXPRESSIONS,
DEMEANOUR,DRESS,POSTU
RE,GAIT,SPEECH.
 The following table shows a mini
mentals state examinations
questionnaire
DIFFERENT PHYSICAL SYMPTOMS
 Dysarthria- localized causes, UMN & LMN, cerebellar dysarthria, myasthenia gravis,
parkinsonism.
 Dysphasia- expressive(motor) caused by injury to Broca's area, receptive(sensory)
caused by Wernicke's area, Global dysphasia caused by injury to both.
Cranial nerves
Occulomotor, Trochlear, Abducens
(CN 3,4&6)
Trigeminal nerve(CN 5)
Facial nerve(CN 7)
Vestibulocochlear nerve(CN 8)
Glossopharnygeal nerve( CN 9)
Accessory spinal nerve(CN 11)
Hypoglossal nerve (CN 12)
Assessment of motor system
 Assessing CNS, PNS, basal ganglia, and cerebellar systems to test for motor
systems.
Assessment occurs in the following ways:
 Stance & gait
 Inspection & palpation of muscles
 Assessment of tone
 Testing of movement & power
 Examination of reflexes
 Testing of coordination
Cerebellar examination
Dysdiadochokinesis
The inability to perform and sustain a series of repeated movements
Ataxia
Gross incoordination of movements – gait
Nystagmus
Repetitive, involuntary oscillation of the eyes
Intention tremor
A wide tremor when performing voluntary movements
Slurred speech
Speech may be imprecise slow and distorted
Hypotonia
The patient may have muscle weakness
Pass pointing (dysmetria)
The patient overshoots when touching the examiners finger
Stance & Gait
 Stance(Standing) & gait (Walk)depends on intact visual, vestibular, sensory,
corticospinal, extrapyramidal along with functioning lower motor neurons and spinal
reflexes.
 Unsteadiness on standing with eyes open suggests cerebellar ataxia.
 Rhombergs test(Unsteadiness on standing with eyes closed ) suggests proprioceptive
sensory loss, bilateral vestibular loss.
Inspection & palpation of muscles
 LMN usually causes muscle wasting whereas UMN usually shows disuse atrophy.
 Muscle disorders usually causes proximal wasting of muscles except myotonic wasting.
 Fasciculations are visible irregular twitching of resting muscles usually caused in LMN
and physiologically in calves.
Abnormal movements
Myoclonic jerks- sudden shock like contractions of one or more muscles that may be
focal or diffuse occur .singly or repeatedly. Pathologically seen in epilepsy, diffuse brain
damage and neurodegenerative disorders.
Tremors
 Tremor is an involuntary, oscillatory movement
about a joint or a group of joint resulting from
contraction and relaxation of muscles.
 Physiological tremors are fine which can be also
seen in hyperthyroidism, excess alcohol or
caffeine intake
 Parkinsonism causes pill rolling tremor
 Isolated heat tremor caused in torticollis
 Intention tremor usually seen in cerebellar
damage.
Tone
 Tone is the resistance felt by the
examiner when moving a joint
passively.
 Hypotonia is usually seen in LMN,
cerebellar disease, early phases of
cerebral or spinal shock.
 Hypertonicity occurs in two forms:
spasticity and rigidity
 Spasticity is velocity dependent
resistance to passive movements,
seen in UMN lesions.
 Rigidity is sustained resistance
throughout the range of movement
and it is more easily detected when
the limb is moved slowly.
Clonus
 Clonus is rhythmic series of
contractions evoked by a sudden
stretch of muscle and tendon.
 Unsustained clonus will be
physiological, but sustained denotes
UMN damage. Best seen in ankle
and knee
Myotonia
 It is described as the inability of muscles to relax normally.
Power of muscles
 UMN lesions produces weakness in a large
group of muscles such as limbs, whereas
LMN produces weakness in a small group
of muscles.
 A tendon reflex is an involuntary
contraction of a muscle in response to
stretch. It is mediated by the reflex arc.
 Reflexes are primitive which are usually
seen in neonates which disappear as
we get older and deep tendon reflexes
which we usually assess.
 Various types of reflexes are: biceps jerk,
triceps jerk, finger jerk, knee jerk, ankle
jerk, plantar jerk
Coordination
Apraxia
 Apraxia/dyspraxia is difficulty or inability to perform a task despite no sensory or motor
abnormalities. It usually denotes disturbance in higher cortical function in non-
dominant parietal or frontal lobe.
Common presenting symptoms
Common presenting symptoms:
 Paraesthesia: tingling, pins or needles.
 Dysaesthesia: unpleasant paraesthesia
 Hypoaesthesia: reduced sensation to normal sensation.
 Analgesia: numbness or loss of sensation
 Hyperaesthesia: increased sensitivity to stimulus.
 Allodynia: painful sensation to a non- painful stimulus.
 Hyperalgesia: increased sensitivity to a painful stimulus.
Peripheral nerve examination
Investigations
 Not necessary , do as and when required
 Perform a basic blood test and then
perform a relevant imaging according to
the case.
 Lumbar puncture – acute and
chronological conditions
 Electroencephalography (EEG)- epilepsy,
encephalopathies or dementia &
Electromyography(EMG)- neurogenic and
myopathic pathologies
 Nerve conduction studies- nerve
conductions and polyneuropathies
Acoustic
neuroma
Delirium
(drugs, metabolic,
CNS/non CNS
infection)
Cranial
arteritis
Acute
glaucoma
UMN v
LMN
Eye v
Brain
1O
V 2O
Infection
Mnemonic – VITAMIN CDE
• V – Vascular
• I – Infective/Inflammatory
• T – Trauma/Toxins
• A - Autoimmune
• M – Metabolic
• I – Iatrogenic/Idiopathic
• N - Neoplastic
• C - Congenital
• D - Degenerative
• E - Endocrine
Differential Diagnoses
Special tests
Pronator drift
Sign of a contralateral UMN lesion
Rombergs test
Proprioception, vestibular function and vision
Normal test requires healthy functioning of the dorsal spinal columns
(proprioception)
Sciatic and femoral stress test
Tinnels/phalens tests
Test for carpal tunnel syndrome – median nerve compression
Swinging light test
Relative afferent pupillary defect (RAPD)
Detect dysfunction in retinal or optic nerve
Retinal detachment, optic nerve damage-raised ICP or MS
https://www.gmc-uk.org/-/media/documents/mla-
content-map-_pdf-85707770.pdf
Infection
Metabolic
Drugs
Epilepsy
Arterial
Trauma
Hypoxia

Nervous system( History & examination of )

  • 1.
    Nervous System History andexamination Dr.Shailesh Kamble( MSc Human Anatomy)
  • 2.
    Overview Aim The session willalso introduce the special features of neurological history taking and examination and the language of neurology. Learning outcomes Describe the special features of the neurological history and examination Define some neurological terms
  • 4.
    Neurons are thebuilding blocks. Astrocytes provide structural framework whereas microglial cells are concerned with immune and scavenging functions. CNS- oligodendrocytes produces myelin sheath PNS- Schwann cells produce myelin sheath. Volume of CSF is around 140-270 ml which is replenished 3 to 4 times in a day with production rate of 700mL/day. Spinal cord contains afferent and efferent pathways which are responsible for motor and sensory information transmission. Sensory cell bodies of peripheral nerves are in the dorsal root ganglion. Motor cell bodies are located in the anterior horn of the spinal cord. General introduction
  • 5.
    History TIME RELATIONSHIP  Forcommon neurological symptoms such as headaches, numbness, loss of consciousness, history is the key to diagnosis.  ALWAYS THINK WHERE IS THE LESION? WHAT IS THE LESION?  Always remember to ask patients to define symptoms in their own language. O- onset(When did the symptom start?/when was he well last time?) (sudden, gradual/evolving) D- duration(Persistent/intermittent) P- progress ( Better or worse or same)
  • 6.
     What wasthe patient doing when the symptoms occurred?(Precipitating factor)  Anything which makes the patient's symptoms better or worse( time of the day, menstrual cycles, posture or medications)(Relieving/exacerbating factors Precipitating, exacerbating or relieving factors
  • 7.
    Associated symptoms  With everydisease you have associated symptoms like in case of headache you will have nausea, vomiting, photophobia( aversion to light) or phonophobia( aversion to sound)
  • 8.
    Presenting complaint inneurology Common Headaches Dizziness Pain Numbness Pins and needles Weakness Others Memory Shaking Vision Confusion Loss of consciousness Questions • Describe it to me? • Frequency? • Location? • Precipitant, exacerbating/alleviating factors? • RED FLAGS • Thunderclap headache • Slurred speech, weakness • Incontinence of bladder/bowels • Bilateral sciatica • Seizures • Acute confusion • Fever • Non blanching rash
  • 9.
    Other histories  PASTMEDICAL HISTORY- Symptoms which patients usually forget, birth history or development history( in epilepsy), or hypertension, diabetes.  DRUG HISTORY- Prescribed, over the counters, complementary or recreational drugs.  FAMILY HISTORY- First degree relatives  SOCIAL HISTORY- Coping with the symptoms, affecting work? Diet history especially vegetarians(VIT B12 intake), alcohol intake, drugs, STDs, travel history  OCCUPATIONAL HISTORY- toxic peripheral neuropathy due to exposure any metals, epilepsy for driving, cognitive levels for dementia.
  • 10.
    PHYSICAL EXAMINATION  Physicalexamination begins when the patient enters the clinic. OBSERVE FACIAL EXPRESSIONS, DEMEANOUR,DRESS,POSTU RE,GAIT,SPEECH.  The following table shows a mini mentals state examinations questionnaire
  • 12.
    DIFFERENT PHYSICAL SYMPTOMS Dysarthria- localized causes, UMN & LMN, cerebellar dysarthria, myasthenia gravis, parkinsonism.  Dysphasia- expressive(motor) caused by injury to Broca's area, receptive(sensory) caused by Wernicke's area, Global dysphasia caused by injury to both.
  • 14.
  • 16.
  • 17.
  • 18.
  • 19.
  • 20.
  • 21.
  • 22.
  • 23.
    Assessment of motorsystem  Assessing CNS, PNS, basal ganglia, and cerebellar systems to test for motor systems. Assessment occurs in the following ways:  Stance & gait  Inspection & palpation of muscles  Assessment of tone  Testing of movement & power  Examination of reflexes  Testing of coordination
  • 24.
    Cerebellar examination Dysdiadochokinesis The inabilityto perform and sustain a series of repeated movements Ataxia Gross incoordination of movements – gait Nystagmus Repetitive, involuntary oscillation of the eyes Intention tremor A wide tremor when performing voluntary movements Slurred speech Speech may be imprecise slow and distorted Hypotonia The patient may have muscle weakness Pass pointing (dysmetria) The patient overshoots when touching the examiners finger
  • 25.
    Stance & Gait Stance(Standing) & gait (Walk)depends on intact visual, vestibular, sensory, corticospinal, extrapyramidal along with functioning lower motor neurons and spinal reflexes.  Unsteadiness on standing with eyes open suggests cerebellar ataxia.  Rhombergs test(Unsteadiness on standing with eyes closed ) suggests proprioceptive sensory loss, bilateral vestibular loss.
  • 28.
    Inspection & palpationof muscles  LMN usually causes muscle wasting whereas UMN usually shows disuse atrophy.  Muscle disorders usually causes proximal wasting of muscles except myotonic wasting.  Fasciculations are visible irregular twitching of resting muscles usually caused in LMN and physiologically in calves.
  • 29.
    Abnormal movements Myoclonic jerks-sudden shock like contractions of one or more muscles that may be focal or diffuse occur .singly or repeatedly. Pathologically seen in epilepsy, diffuse brain damage and neurodegenerative disorders.
  • 30.
    Tremors  Tremor isan involuntary, oscillatory movement about a joint or a group of joint resulting from contraction and relaxation of muscles.  Physiological tremors are fine which can be also seen in hyperthyroidism, excess alcohol or caffeine intake  Parkinsonism causes pill rolling tremor  Isolated heat tremor caused in torticollis  Intention tremor usually seen in cerebellar damage.
  • 31.
    Tone  Tone isthe resistance felt by the examiner when moving a joint passively.  Hypotonia is usually seen in LMN, cerebellar disease, early phases of cerebral or spinal shock.  Hypertonicity occurs in two forms: spasticity and rigidity  Spasticity is velocity dependent resistance to passive movements, seen in UMN lesions.  Rigidity is sustained resistance throughout the range of movement and it is more easily detected when the limb is moved slowly.
  • 33.
    Clonus  Clonus isrhythmic series of contractions evoked by a sudden stretch of muscle and tendon.  Unsustained clonus will be physiological, but sustained denotes UMN damage. Best seen in ankle and knee
  • 34.
    Myotonia  It isdescribed as the inability of muscles to relax normally.
  • 35.
    Power of muscles UMN lesions produces weakness in a large group of muscles such as limbs, whereas LMN produces weakness in a small group of muscles.  A tendon reflex is an involuntary contraction of a muscle in response to stretch. It is mediated by the reflex arc.  Reflexes are primitive which are usually seen in neonates which disappear as we get older and deep tendon reflexes which we usually assess.  Various types of reflexes are: biceps jerk, triceps jerk, finger jerk, knee jerk, ankle jerk, plantar jerk
  • 37.
  • 38.
    Apraxia  Apraxia/dyspraxia isdifficulty or inability to perform a task despite no sensory or motor abnormalities. It usually denotes disturbance in higher cortical function in non- dominant parietal or frontal lobe.
  • 39.
    Common presenting symptoms Commonpresenting symptoms:  Paraesthesia: tingling, pins or needles.  Dysaesthesia: unpleasant paraesthesia  Hypoaesthesia: reduced sensation to normal sensation.  Analgesia: numbness or loss of sensation  Hyperaesthesia: increased sensitivity to stimulus.  Allodynia: painful sensation to a non- painful stimulus.  Hyperalgesia: increased sensitivity to a painful stimulus.
  • 40.
  • 41.
    Investigations  Not necessary, do as and when required  Perform a basic blood test and then perform a relevant imaging according to the case.  Lumbar puncture – acute and chronological conditions  Electroencephalography (EEG)- epilepsy, encephalopathies or dementia & Electromyography(EMG)- neurogenic and myopathic pathologies  Nerve conduction studies- nerve conductions and polyneuropathies
  • 42.
  • 44.
  • 45.
    Mnemonic – VITAMINCDE • V – Vascular • I – Infective/Inflammatory • T – Trauma/Toxins • A - Autoimmune • M – Metabolic • I – Iatrogenic/Idiopathic • N - Neoplastic • C - Congenital • D - Degenerative • E - Endocrine Differential Diagnoses
  • 46.
    Special tests Pronator drift Signof a contralateral UMN lesion Rombergs test Proprioception, vestibular function and vision Normal test requires healthy functioning of the dorsal spinal columns (proprioception) Sciatic and femoral stress test Tinnels/phalens tests Test for carpal tunnel syndrome – median nerve compression Swinging light test Relative afferent pupillary defect (RAPD) Detect dysfunction in retinal or optic nerve Retinal detachment, optic nerve damage-raised ICP or MS
  • 47.