Professional Documents
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CNS
CNS
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• Astrocytes = control the environment and form the blood–brain barrier.
• Microglial cells = blood-derived mononuclear macrophages.
• Oligodendrocytes = produce myelin sheath in the CNS
• Schwann cells = produce myelin sheath in the PNS.
• Between the brain and the skull are 3 meninges = dura mater, arachnoid and pia mater.
• The subarachnoid space is filled with CSF.
• Sensory cell bodies are situated in the dorsal root ganglia.
• The motor cell bodies are in the ant. horns of the spinal cord
The onset, duration and pattern of symptoms over time often provide
diagnostic clues: for example, in assessing headache or vertigo.
• Headache is the most common neurological symptom and may be either primary or secondary to other pathology.
• Orbital/retro-orbital; always same side during cluster, may switch sides between clusters.
• Abrupt onset, attacks last up to 2hrs. Recurrent attacks 1-4x within 24hrs, lasting weeks to months.
• Awakes the patient from sleep
• Autonomic features (conjunctival injection, tearing, nasal stuffiness, ptosis, miosis, agitation).
• During the attack the patient keep pacing around the room in an agitated state, or even head banging.
• Common, often more frequent than epilepsy, sometimes occurring multiple times in a day,
and may last considerably longer, with symptoms waxing and waning.
• Other features include asynchronous movements, pelvic thrusts, side-to-side rather than
flexion/extension movements and absence of postictal confusion.
• A stroke is a focal neurological deficit of rapid onset that is due to a vascular cause, can be ischemic or hemorrhagic.
• TIA is the same but symptoms resolve within 24hrs.
• 80% of strokes are ischemic. Hemorrhagic stroke is much more frequent in Asian populations. We do brain CT w/o contrast to differentiate b/w them.
• Factors in the history or examination that increase the likelihood of hemorrhage rather than ischemia include use of anticoagulation, headache,
vomiting, seizures and early reduced consciousness.
• Very rare; present with an abrupt onset, depending on the level of spinal cord affected.
• The ant. spinal artery syndrome is most common and causes loss of motor function and pain/temp. sensation with
relative sparing of joint position and vibration sensation below the level of the lesion (sparing dorsal column).
• Neurological Sx that are not due to disease are called ‘functional’ but other terms include psychogenic, hysterical, somatisation or conversion disorders.
• Sx include: blindness, tremor, weakness and collapsing attacks, with fatigue, lethargy, pain, anxiety, etc.
A history of previous visual loss in someone presenting with numbness suggests multiple sclerosis
• Alcohol is the most common toxin and damages both the CNS (ataxia, seizures, dementia) and the PNS (neuropathy). Alcoholism may cause vitamin deficiency.
• Vegetarians may be susceptible to vitamin B12 deficiency. Nitrous oxide inhalation causes subacute combined degeneration of the cord due to vit. B12 pathway dysfunction.
• A travel history may give clues to the underlying diagnosis, such as Lyme disease (facial palsy), neurocysticercosis (brain lesions and epilepsy) or malaria (coma).
Note: the ex. sequence for OSCE purposes was provided by the doctors; you can ignore the ex. attached figures here and consider it only for understanding of the OSCE steps maneuvers
• The posterior part of the frontal lobe is the precentral gyrus, which controls voluntary movement.
• The area anterior to the precentral gyrus is concerned with personality, social behavior, emotions,
cognition, expressive language, frontal eye fields and cortical center for micturition.
• It contains the primary auditory cortex, Wernicke’s area and parts of the limbic system.
• It also contains the lower fibers of the optic radiation and the area of auditory perception.
• The limbic system is important in memory, emotion and smell appreciation.
• The postcentral gyrus is the most ant. part of the parietal lobe and is the destination
of sensations. The upper fibers of the optic radiation pass through it.
• The dominant hemisphere contains aspects of language function and the
non-dominant lobe is concerned with spatial awareness.
• Irregular twitches under the skin overlying resting muscles caused by individual
motor units firing spontaneously, occurring in LMN diseases, usually in wasted
muscles. It is seen, not felt.
• Physiological fasciculation is common, especially in the calves.
• Myokymia is rapid bursts of repetitive motor unit activity often occurring in an
eyelid or first dorsal interosseus, and is rarely pathological.
• Dystonia = sustained muscle contractions, leading to twisting, repetitive movements and sometimes tremor. It
may be focal (as in torticollis), segmental (affecting two or more adjacent body parts) or generalized.
• Chorea = brief, random, purposeless movements which may affect various body parts, but commonly the arms.
• Athetosis = slower, writhing movement, more similar to dystonia than chorea.
• Ballism = violent flinging movements sometimes affecting only one side of the body (hemiballismus).
• Tics = repetitive, stereotyped movements which can be briefly suppressed by the patient.
• LMN lesions, usually ass. with muscle wasting, weakness and hyporeflexia.
• Found in cerebellar disease or signal the early phases of cerebral or spinal shock.
• Sustained resistance throughout the range of movement; detected when the limb is moved slowly.
• In parkinsonism, this is classically described as ‘lead pipe rigidity’.
• In the presence of a parkinsonian tremor there may be a regular interruption to the movement,
giving it a jerky feel (cog wheeling).
• Rhythmic series of contractions evoked by sudden stretch of the muscle and tendon.
• Unsustained (<6 beats) clonus may be physiological. When sustained, it indicates UMN damage,
• Caused by combined spinal cord and root pathology localizing to a specific spinal level.
• It is most common at the C5/6 level. When elicited, the biceps reflex is absent or
reduced but finger flexion occurs.
• It is most commonly seen in cervical spondylotic myeloradiculopathy.
In cerebellar disease, the reflexes may be pendular due to slow muscle contraction
and relaxation, however, they are not sensitive or specific cerebellar signs.
• They are lost in UMN lesions but are also affected by LMN damage affecting T8–12.
• They are usually absent in the obese, the elderly or after abdominal surgery.
• In disorders predominantly affecting midline cerebellar structures, truncal ataxia may be the only finding.
• In the most severe cases, the patient cannot sit unsupported.
• Tandem gait (heel–toe walking) may be impaired in less severe cases.
• Weakness may produce false-positive finger-to-nose test, so demonstrate that power is normal first.
• Dysmetria or past-pointing = tendency to fall short or overshoot the examiner’s finger.
• Intention tremor = in more severe cases there may be a tremor of the finger as it approaches the
target finger and the patient’s own nose.
• Dyssynergia = the movement may be slow, disjointed and clumsy
• It is abnormal if the heel wavers away from the line of the shin.
• Weakness may produce false-positive heel-to-shin test, so
demonstrate that power is normal first.
• It is difficulty or inability to perform a task, despite no impairment of the necessary individual functions.
• It is a sign of higher cortical dysfunction, usually localising to the non-dominant frontal or parietal lobes.
Ass. with spatial disorientation and neglect. Usually due to non-dominant hemisphere parietal lesions.
• Conveyed in large, myelinated fast-conducting fibres in the peripheral nerves and in the
posterior columns of the spinal cord
• The posterior column remains ipsilateral from the point of entry up to the medulla.
• Carried by small, slow-conducting fibres of the peripheral nerves and the spinothalamic tract of the spinal cord.
• Most pain and temperature fibres cross to the contralateral spinothalamic tract within one or two segments of
entry to the spinal cord.
All sensory fibres relay in the thalamus before sending information to the sensory cortex in the parietal lobe
• Guillain–Barré syndrome = vibration and joint position sense may be disproportionately affected.
• Patients may report staggering when they close their eyes during hair washing or in the dark (Romberg’s sign).
• Patients may report staggering when they close their eyes during hair washing or in the dark (Romberg’s sign).
• When joint position sense is affected in the arms, pseudoathetosis may be demonstrated by asking the patient
to close their eyes and hold their hands outstretched; the fingers/arms will make involuntary, slow, wandering
movements, mimicking athetosis.
• Traumatic and compressive spinal cord lesions cause loss or impairment of sensation in a dermatomal distribution below the level of the lesion.
• A zone of hyperaesthesia may be found immediately above the level of sensory loss.
• Anterior spinal artery syndrome = Results in loss of spinothalamic sensation and motor function, with sparing of dorsal column sensation.
• A similar dissociated pattern of pain and temperature loss and sparing of dorsal column sensation occurs in syringomyelia.
• Brown-Séquard syndrome = When one-half of the spinal cord is damaged. This is characterized by ipsilateral motor weakness and loss of
vibration and joint position sense, with contralateral loss of pain and temperature.
• Thalamic lesions may cause a patchy sensory impairment on the opposite side with unpleasant, poorly localised
pain, often of a burning quality.
• Cortical parietal lobe lesions typically cause sensory inattention but may also affect joint position sense,
two-point discrimination, stereognosis (tactile recognition) and localisation of point touch.
• Lower brainstem lesions may cause ipsilateral numbness on one side of the face (V nerve nucleus) and
contralateral body numbness (spinothalamic tract).
• Carpal tunnel syndrome is the most common entrapment neuropathy and occurs commonly during pregnancy.
• It may be compressed as it passes between the flexor retinaculum and the carpal bones at the wrist, initially
producing sensory symptoms.
Most often affected at the elbow by external compression, or by injury, as in elbow dislocation/fracture.
Compression usually occurs as the nerve passes through the condylar groove behind the medial epicondyle
or as it passes through the cubital tunnel.
May be compressed as it runs through the axilla, in the spiral groove of the humerus (Saturday night palsy),
or may be injured in fractures of the humerus. It typically causes wrist drop.
It may be damaged in fibular head fractures, or compressed particularly in thin, immobile patients,
or as a result of repetitive kneeling or squatting. This typically presents with foot drop.
This purely sensory nerve may be compressed as it passes under the inguinal
ligament, producing paraesthesiae in the lateral thigh (meralgia paraesthetica).
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• Bipolar cells in the olfactory bulb form olfactory filaments with small
receptors projecting through the cribriform plate high in the nasal cavity.
• These cells synapse with second-order neurons, which project centrally
via the olfactory tract to the medial temporal lobe and amygdala.
• Hyposmia-anosmia = (reduction or loss of the sense of smell) may result from URTI,
sinus disease, damage to the olfactory filaments after head injury or infection, local
compression (olfactory groove meningioma) or invasion by basal skull.
• Disturbance of smell= very early in Parkinson’s and Alzheimer’s diseases.
• Patients often note hypogeusia/ageusia (altered taste) with anosmia too.
• Parosmia is the perception of pleasant odors as unpleasant; it may occur with head
trauma or sinus infection or be an adverse effect of drugs.
• Olfactory hallucinations may occur in Alzheimer’s disease and focal epilepsies.
• The cell bodies of the sensory fibers are in the trigeminal (Gasserian) ganglion, which
lies in a cavity (Meckel’s cave) in the petrous temporal dura.
• From the trigeminal ganglion, the V nerve passes to the pons. From here, pain and
temperature pathways descend to the C2 segment of the spinal cord, so ipsilateral
facial numbness may occur with cervical cord lesions.
• It has three major branches: Ophthalmic (V1), Maxillary (V2) and Mandibular (V3).
• From its motor nucleus in the lower pons, fibers of the VII nerve pass back to loop around the VI nerve
nucleus before emerging from the lateral pontomedullary junction in close association with the VIII nerve;
together they enter the internal acoustic meatus.
• At the lateral end of the meatus, the VII nerve continues in the facial canal within the temporal bone,
exiting the skull via the stylomastoid foramen.
• Passing through the parotid gland, it gives off its terminal branches. In its course in the facial canal it gives
off branches to the stapedius muscle and its parasympathetic fibers, as well as being joined by the taste
fibers of the chorda tympani.
• Sends motor fibers to the muscles of facial expression (frontalis, orbicularis oculi, buccinators,
orbicularis oris and platysma).
• Send parasympathetic fibers to the lacrimal, submandibular and sublingual salivary glands.
• Receives taste sensation from the anterior 2/3 of the tongue.
• Unilateral LMN VII nerve lesion (lesions distal to the stylomastoid foramen / damage of
the facial nerve in the facial canal) = weakness of both upper and lower facial muscles.
• Ramsay Hunt syndrome = herpes zoster infection of the geniculate (facial) ganglion.
This produces a severe LMN facial palsy, ipsilateral loss of taste and buccal ulceration,
and a painful vesicular eruption in the external auditory meatus.
• Other causes of a LMN VII lesion = cerebellopontine angle tumors (including acoustic
neuroma), trauma and parotid tumors.
• Unilateral VII nerve UMN lesions = weakness is marked in the lower facial muscles with
relative sparing of the upper face. The nasolabial fold may be flattened, and the corner of
the mouth drooped, but eye closure is usually preserved.
• Hemifacial spasm = synchronized twitching of the ipsilateral eye and mouth.
• Bilateral facial palsies are less common, but occasionally occur, as in Guillain–Barré
syndrome, sarcoidosis, or infection such as Lyme disease, HIV or leprosy.
• Facial weakness, especially with respect to eye closure = in some congenital myopathies
(facioscapulohumeral or myotonic dystrophies).
• Parkinson’s disease = loss of spontaneous facial movements, including a slowed blink
rate, and involuntary facial movements (levodopa-induced dyskinesias) may complicate
advanced disease.
• Both nerves arise as several roots from the lateral medulla and leave the skull together
via the jugular foramen.
• The IX nerve passes down and forwards to supply the stylopharyngeus muscle, the
mucosa of the pharynx, the tonsils and the posterior one-third of the tongue, and sends
parasympathetic fibers to the parotid gland.
• The X nerve courses down in the carotid sheath into the thorax, giving off several
branches, including pharyngeal and recurrent laryngeal branches, which provide motor
supply to the pharyngeal, soft palate and laryngeal muscles.
• The main nuclei of these nerves in the medulla are the nucleus ambiguous (motor), the
dorsal motor vagal nucleus (parasympathetic) and the solitary nucleus
• Isolated unilateral IX nerve lesions are rare. Unilateral X nerve damage = ipsilateral reduced
elevation of the soft palate, causing deviation of the uvula (away from the side of the lesion).
• Unilateral lesions of IX and X are most caused by strokes, skull-base fractures or tumors.
• Damage to the recurrent laryngeal branch of the X nerve due to lung cancer, thyroid surgery,
mediastinal tumors and aortic arch aneurysms = dysphonia and a ‘bovine’ cough.
• Bilateral X nerve lesions = dysphagia and dysarthria that may be due to lesions at the UMN le
(pseudobulbar palsy) or LMN level (bulbar palsy). Less severe cases can result in nasal regurgita
of fluids and nasal air escape when the cheeks are puffed out.
• Always consider myasthenia gravis in patients with symptoms of bulbar dysfunction, even if th
examination seems normal.
• The accessory nerve has two components;
1- A cranial part; closely related to the vagus
2- A spinal part (C1-5); which provides fibers to the upper trapezius (shoulder shrugging) and SCM muscles (he
• The spinal nuclei arise from the anterior horn cells of C1–5. Fibers emerge from the spinal cord, ascend through
magnum and exit via the jugular foramen, passing posteriorly.
• Wasting of the upper fibers of trapezius = displacement (winging) of upper border of the scapula away
from the spine, and the lower border is displaced towards it.
• Wasting and weakness of the SCM = dystrophia myotonica.
• Weakness of neck muscles (Head drop) = myasthenia, motor neuron disease, and some myopathies.
• Dystonic head postures causing antecollis (neck flexed), retrocollis (neck extended) or torticollis (neck
twisted to one side) are not associated with weakness.
• The nucleus lies in the dorsal medulla beneath the floor of the fourth ventricle.
• The nerve emerges anteriorly and exits the skull in the hypoglossal canal, passing
to the root of the tongue supplying its muscles.
• Unilateral LMN lesions = wasting of the tongue on the affected side and deviation to that side on protrus
• Bilateral LMN lesion results in global wasting, and involuntary twitching (Fasciculation).
• Bilateral UMN lesions = Spastic tongue and the patient has difficulty flicking the tongue from side to sid
• Tremor of the resting or protruded tongue = in Parkinson’s disease, although jaw tremor is more commo
• Other orolingual dyskinesias (involuntary movements of the mouth and tongue) are often drug-induced
include tardive dyskinesias due to neuroleptics.
Bulbar palsy refers to impairment of function of the cranial nerves IX, X, XI and XII, which
occurs due to a lower motor neuron lesion either at nuclear or fascicular level in the
medulla oblongata or from lesions of the lower cranial nerves outside the brainstem.
• The eye is protected by the eyelid, which affords protection and maintains the tear film.
• Upper lid elevation = levator palpebrae superioris (innervated by the 3rd CN), and Müller’s muscle, (innervated by the sympathetic ANS).
• Eyelid closure = orbicularis oculi muscle (innervated by 7th CN).
• The orbit also contains the 6 extraocular muscles. In addition, the orbit houses the lacrimal gland, blood vessels, autonomic nerve fibers
and CN 2, 3, 4, and 6. The contents are cushioned by orbital fat, which is enclosed anteriorly by the orbital septum and the eyelids.
• The conjunctiva is a thin mucous membrane lining the posterior aspects of the eyelids. It is reflected at the superior and inferior fornices
on to the surface of the globe. It is coated in a tear film that protects and nourishes the ocular surface.
• The cranial nerves originate in the midbrain and pons and then pass through the cavernous sinus.
The 6 extraocular muscles (superior rectus, medial rectus, lateral rectus, inferior rectus muscles, inferior oblique,
and superior oblique muscle) are responsible for eye movements. All are innervated by CN 3, except superior
oblique by CN 4 and lateral rectus by CN 6.
The visual pathway consists of the retina, optic nerve, optic chiasm, optic tracts, lateral geniculate bodies, optic
radiations and visual cortex. Deficits in the visual pathway lead to specific field defects as attached.
• Afferent pathway = involves the optic nerve, chiasm (where some fibers decussate) and the optic tract,
bypassing the lateral geniculate nucleus, synapsing in the pretectal nucleus of the midbrain then terminate
in the III nerve (Edinger–Westphal) nucleus and then pass along the inferior division of the oculomotor
nerve to synapse in the ciliary ganglion.
• Efferent pathway = involves the inferior division of the III nerve, passing through the ciliary ganglion in the
orbit to the constrictor muscle of the iris via short ciliary nerves, resulting in constriction.
• The sympathetic pathway originates in the hypothalamus, passing down to the ciliospinal center of Budge at th
level of T1.
• Fibers then pass to, and synapse in, the superior cervical ganglion before joining the surface of the internal caro
artery and passing to the pupil along the nasociliary and the long ciliary nerves.
• If the degree of anisocoria is greater in brighter lighting, then it is the larger (dilated) pupil that is abnormal.
• If it is more pronounced in dim lighting, the smaller (constricted) pupil is the abnormal.
• An equal degree of anisocoria in all levels of lighting indicates physiological anisocoria.
• It is an important clinical sign that occurs when disease of the retina or optic nerve reduces the response of the eye to a light st
• In normal patients, this results in symmetrical constriction of both pupils.
• In RAPD, light in the affected eye causes weaker constriction (apparent dilatation) compared to light shone in the normal eye.
• It results from dysfunction of sympathetic nerve supply to the eye, which originates in the hypothalamus and emerges in the root of the neck
before innervating the pupil. Damage at any point in this pathway will result in Horner’s syndrome.
• On examination, there is a constricted pupil (loss of sympathetic dilator tone) and a partial ptosis resulting from denervation of Müller’s musc
the upper eyelid. There may also be anhydrosis (loss of sweating) on the affected side.
• Thus, Horner syndrome is triad of anhydrosis, partial ptosis and miosis.
• Diagnosis may be confirmed by cocaine eye drops, which will cause pupil dilatation in the unaffected pupil but no dilatation on the affected s
• Causes of Horner’s syndrome include demyelination, neck trauma/surgery, apical lung tumor (Pancoast tumour) and carotid artery dissection
• This is a benign, mid-dilated pupil that responds poorly to both light and accommodation. With time, however, the affected pupil can become cons
• It is thought to result from parasympathetic pathway dysfunction in the orbit.
• It typically affects young women.
• When associated with diminished Achilles tendon reflexes, it is referred to as Holmes–Adie syndrome.
• Bilateral small, irregular pupils that reacts to accommodation (constrict on a near object) but not
light (do not constrict when exposed to bright light).
• This is classically the result of neurosyphilis. There are other causes of light-near dissociation,
however, including DM, severe optic nerve disease and midbrain lesions.
• Starts from retina > optic nerve > the optic chiasm > optic tract > optic radiation > occipital cortex.
• The nasal fibers of the optic nerve are responsible for the temporal visual field and vice versa.
• It is purely sensory; responsible for transmitting visual sensory information from the retina to the brain
• It is the afferent part of the pupillary reflex and is unable to regenerate.
• Before the Optic chiasm = The visual field loss is seen on the same (ipsilateral) side as the lesion.
• After the optic chiasm = The visual loss is seen on the opposite (contralateral) side of the lesion;
because the optic nerves have already crossed over at the optic chiasm.
• Supplies the lateral rectus muscle and abducts the eye (lateral gaze).
• Has along course around the brainstem before it pierces the dura to enter the cavernous sinus.
• In direct relation to the internal carotid artery before it passes through the superior orbital
fissure to the lateral rectus muscle.