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Nervous system
Letuda’s note
Version 2.
Written, edited and digitalized by
Prithwiraj Maiti
Final year MBBS (Batch 2015)
R.G.Kar Medical College
Table of contents
Contents Page no.
Introduction to CNS
Contents: UMN lesion, LMN lesion, Corticospinal fibres,
Corticonuclear fibres, Specialty of facial nerve, Localization
of corticospinal tract lesion
Cranial nerves
Contents: CN1, CN2, Optic neuritis, CN3, CN4, CN6, Ptosis,
Squint, Light reflex, Accommodation reaction, CN5,
Corneal reflex, Trigeminal neuralgia, CN7, Bell’s palsy, CN8,
CN 9,10,11,12; Bulbar and pseudobulbar palsy, CN
Examination of nervous system: General topic
Contents: Higher function, Motor function (tone, power,
reflex), Sensory function, Sensory-motor coordination
Spinal cord
Contents: Myelopathy, Compressive myelopathy,
Complete/ partial cord compression, Extramedullary/
intramedullary compression, Paraplegia in flexion/
extension, Chronic cord compression, Dx of cord
compression; Non-compressive myelopathy, Acute
transverse myelitis, Motor neurone disease, Amyotrophic
lateral sclerosis.
Cerebrovascular accidents (CVA)
Contents: Transient ischemic attack (TIA), Stroke, Lacunar
infarct, Brainstem signs, Subarachnoid hemorrhage (SAH),
Saccular aneurysm.
Neuropathies
Contents: GB syndrome, Miller-fisher syndrome, Polio,
Peripheral
neuropathy, Myasthenia gravis, Lambert-Eaten
Myasthenia Syndrome
Miscellaneous topics
Contents: Subacute combined degeneration of spinal cord,
Fredrick’s ataxia, Tabes dorsalis, Multiple sclerosis,
Parkinsonism, Conus medullaris and Cauda equina lesions.
Myopathy
Contents: Myopathy in general, Myotonic dystrophy,
Duchenne’s muscular dystrophy, Becker’s muscular
dystrophy.
Infective diseases of CNS
Contents: Pyogenic meningitis, Tubercular meningitis,
Brain abscess.
Brain tumor, seizure and related topics
Contents: Brain tumor, Pseudotumor cerebri/ Benign
intracranial hypertension (BIH), Seizure, Status epilepticus.
Syncope and headache
Contents: Syncope, Headache, Migraine, Tension
headache, Cluster headache.
Extras
Contents: Involuntary movements (Tremor, Chorea,
Athetosis, Fasciculation), Dementia
Actions of UMN and LMN:
Through upper motor neurons, cortex exerts a negative control over the
lower motor neurons. So, the main function of UMN is control of voluntary
movements.
The main function of LMN is control of muscle movements.
Basic feature of UMN and LMN lesions:
UMN lesion: Loss of voluntary movement
LMN lesion: Paralysis of muscle.
Details of features of UMN and LMN lesions:
Points UMN lesion* LMN lesion*
Muscle power Decreased
Muscle tone Hypertonia/ spasticity Hypotonia/ flaccidity
Wasting/ atrophy of
muscles
Absent Present
(due to denervation)
Deep tendon reflex (DTR)/
Jerk/ Stretch reflex
Exaggerated
(clonus may be present)
Absent
Superficial reflex Planter: Extensor
Other reflexes: Lost
Plantar: Unresponsive
Other reflexes: Lost
Above signs will be present in that part of the body which is innervated by the affected/
damaged UMN/LMN.
*UMN may be described as the overhead wire over the railways and LMN may be
described as the rail track. If the overhead wire gets cut, there is still a chance of
running the train by other methods (like motor/ diesel etc.) but if the rail track is
damaged, there is no way to run the train.
Just like that, if UMN is damaged, the muscles can still work (and in reality they
work with hyperactivity due to loss of cortical control) but if LMN is damaged, the
muscles can’t work at all and they become flaccid, atrophied with loss of all
reflexes.
Corticospinal fibres
Course
This level is
very important
Corticospinal fibres
They arise from cortex and ultimately innervate different motor cranial
nerve nuclei in the brainstem, forming UMN pathway of that particular
cranial nerve.
Therefore, all of the motor cranial nerve nuclei are bilaterally innervated by
corticonuclear fibres ( except lower half of 7th^ cranial nerve nucleus ).
The case of 7th^ cranial nerve corticonuclear fibres
CN7 nucleus has an upper ½ and a lower ½ from which, upper and lower ½
of facial muscles are innervated.
Corticonuclear fibres of the upper ½ of the CN7 nucleus act exactly like the
other motor cranial nerve nuclei. Therefore , upper ½ of CN7 nucleus is
innervated by corticonuclear fibres from both side of motor cortex.
But, corticonuclear fibres destined for lower ½ of CN7 nucleus leave rest of
the pyramidal fibres at the level of midbrain and decussate to innervate the
nuclei.
Therefore, lower ½ of CN7 nucleus has got unilateral corticonuclear
innervation which comes from contralateral side.
Localization of corticospinal tract lesion (compare with the pictures above)
Site Structure damaged Effect
Cortex
Corticospinal tract Contralateral hemiplegia
Corticonuclear fibre innervating
lower ½ of CN7 nucleus
Paralysis of contralateral lower ½ of
face (UMN type CN7 palsy)
Higher cortical areas Higher cortical dysfunction
(Ex: speech area damage: aphasia)
Fibres of visual field Visual field defect
Because the pyramidal fibres are widely separated in cortex, a cortical
lesion often causes isolated monoparesis/ asymmetrical weakness of the
limbs/ weakness of contralateral lower ½ of face.
Internal
capsule
Corticospinal tract Contralateral hemiplegia
Corticonuclear fibre innervating
lower ½ of CN7 nucleus
Paralysis of contralateral lower ½ of
face (UMN type CN7 palsy)
Midbrain Corticospinal tract Contralateral hemiplegia
Corticonuclear fibre innervating
lower ½ of CN7 nucleus
Paralysis of contralateral lower ½ of
face (UMN type CN7 palsy)
CN3 nucleus Ipsilateral LMN type CN3 palsy
CN4 nucleus Ipsilateral LMN type CN4 palsy
Pons Corticospinal tract Contralateral hemiplegia
Corticonuclear fibre innervating
lower ½ of CN7 nucleus
Paralysis of contralateral lower ½ of
face (UMN type CN7 palsy)
CN6 nucleus Ipsilateral LMN type CN6 palsy
Principal sensory nucleus of CN5 Loss of touch sensation from
ipsilateral ½ of face
Sympathetic trunk Ipsilateral Horner’s syndrome
Lateral spinothalamic tract Loss of pain and temperature
sensation from contralateral ½ of body
Medulla Corticospinal tract Contralateral hemiplegia
CN 9,10,11,12 nucleus LMN type bulbar palsy
Sympathetic trunk Ipsilateral Horner’s syndrome
Lateral spinothalamic tract Loss of pain and temperature
sensation from contralateral ½ of body
Spinal nucleus of CN5 Loss of pain and temperature
sensation from ipsilateral ½ of face
(White: Lost field of vision) Lesions at different levels and their effects
Level of lesion Effect Optic nerve Monocular loss of vision from both the fields of the affected side In the affected eye: Direct light reflex (DLR): Absent Consensual light reflex (CLR): Preserved
- This defect is called RAPD (Relative afferent pupillary defect)/ Marcus Gunn Pupil. Optic chiasma Bitemporal hemianopia (both temporal fields are lost) Some of the important causes are: Pituitary tumor Supra-sellar tumor Craniopharyngioma. Optic tract, LGB and optic radiation lesion: Homonymous hemianopia (identical half of the visual field of each eye is lost), crossed/ contralateral in types (as the contralateral half of the visual field is lost).
Optic tract Congruous in type (as the fibres within optic tract are densely arranged; when the visual field loss is mapped out, they look symmetrical/ identical). Optic radiation Congruous in type (The fibres within optic radiation are widely separated, but the fibres responsible for superior and inferior quadrantic vision group together and pass through parietal and temporal lobes, respectively).
Optic neuritis (SN) Introduction
Inflammation of optic nerve.
Etiology
- Multiple sclerosis (MS)
- Viral infection
- Devic’s disease. Clinical features
- Monocular loss of vision
- Orbital/ retro-orbital pain, particularly on upward gaze due to inflammation of the superior rectus tendon
- Loss of vision from nasal as well as temporal field
- Affected eye: DLR lost but CLR present. Investigation
MRI orbit
Treatment
High dose corticosteroid
CN3, CN4 and CN Function
- Innervate extraocular muscles and thereby mediate movement of eyeball. Innervation of EOM: [ALL]3 [SO]4 [LR]
Some important causes of CN3, CN4 and CN6 palsy
Causes of CN3 palsy Group Cause Diseases of midbrain CVA Tumor Abscess Meningeal diseases In bacterial meningitis, the inflammatory exudate often strangulate the nerve at the basal meninges. Diseases of Subarachnoid space
Hemorrhage: Particularly in aneurysm of posterior communicating artery (PCA). Diseases of Cavernous sinus
Cavernous sinus thrombosis Carotid-cavernous fistula Lateral extension of pituitary (uncommon). Orbital diseases Tumor Cellulitis. Others Mononeuritis multiplex (secondary to diabetes and vasculitis)
Causes of CN4 palsy (rare)
- Head injury
- Midbrain diseases
- Meningeal diseases
- Cavernous sinus diseases
- Orbital diseases. [Point 2-5 are same as CN3 palsy] Causes of CN6 palsy
- Raised ICT: As CN6 has the longest intracranial course, fibres often get stretched when ICT raises; giving rise to some false localizing signs in addition to specific signs of CN6 palsy.
- Pontine lesion (as the nucleus of CN6 lies in the pons)
- Meningeal diseases
- Cavernous sinus diseases
- Orbital lesions
- Mononeuritis multiplex. [Points 3-6 are same as CN3 palsy]
Some short notes related to CN3, 4 and 6 Ptosis (SN) Introduction
Drooping of upper eyelid.
Causes of ptosis
CN3 palsy
Damage to nucleus
Damage to nerve fibre
Horner's syndrome
Sympathetic trunk damage
Muller's muscle palsy
Myasthenia gravis
Pathology in N-M junction
Ocular myopathy
Weakness of mucle itself
In Myotonic dystrophy
Note: Parasympathetic fibres (which constricts pupil) pass along CN3 fibres and therefore, often damaged in CN3 nerve lesions.
Loss of light reflex
Causes:
- Optic nerve lesion
- Optic tract lesion (pre-geniculate lesion): The affected eye in this case is called “ Wernicke’s hemianopic pupil ”: DLR is lost in this eye when light is thrown from nasal half, but DLR is present when light is thrown from temporal half. (Remember- W:DT) In contralateral eye: DLR is lost when light is thrown from temporal half and DLR is present when light is thrown from nasal half.
- CN3 palsy
- Argyll Robertson Pupil (SN): It is an abnormality of pupil usually seen in patients of neurosyphilis. Component: a. Usually bilateral b. Pupil is small in size and dilates poorly to mydriatics
c. Light reflex is lost d. Accommodation reaction: Present (Remember: ARP in ARP).
Accommodation reaction
Component:
- Medial convergence of eyeball
- Pupillary constriction
- Anterior-posterior bulging of lens.
Lost accommodation reaction:
Seen in CN3 palsy (as CN3 supplies both medial rectus and constrictor pupillae).
CN
Functions:
- Motor function: Innervates masticatory muscles: a. Temporalis b. Masseter c. Pterygoid.
- Sensory function: Carries superficial sensation from ipsilateral half of face through 3 branches: a. Ophthalmic b. Maxillary c. Mandibular.
- Reflex: CN5 mediates the following reflexes: a. Corneal reflex b. Jaw jerk.
- Loss of corneal reflex.
Causes of CN5 palsy
- Brainstem lesion: CVA a. Pontine lesion: Motor paralysis Touch sensation lost
b. Medullary lesion: Pain sensation lost Temperature sensation lost
- Posterior fossa lesion: CP angle tumor (Acoustic neuroma)
- Trigeminal ganglion lesion: a. Tumor b. Trauma c. Gradenigo’s syndrome
- Cavernous sinus pathology: Thrombosis.
Trigeminal neuralgia (SN) Introduction
It is a condition characterized by excruciating pain along the distribution of trigeminal nerve.
Etiology
- Idiopathic
- Multiple sclerosis
- Intracranial space occupying lesion (IC-SOL): Tumor stretches the nerve fibres
- In some cases, the nerve gets irritated by an aberrant blood vessel. Clinical features
Pain:
a. Site: Usually hemifacial pain, particularly in the chick and chin b. Nature: Severe, often electric shock like pain and typically paroxysmal c. Triggering factor: Often triggered by face washing, shaving, chewing d. The pain is so severe that it throws the face; causing facial spasm and the patient involuntarily starts wincing like a tic ; therefore the condition is also called Tic douloureux . [ It has been described as among the most painful conditions known to humankind.]
