Week 12 Neuro Flashcards
What are cranial nerves?
12 pairs of nerves that exit brainstem which supply face and neck
Sensory, motor and parasympathetic activity
Cranial nerves and their components
CN I Olfactory S
CN II Optic S
CN III Oculomotor M (parasym)
CN IV Trochlear M
CN V Trigeminal B
CN VI Abducens M
CN VII Facial B (parasym)
CN VIII Vestibulocochlear S
CN IX Glossopharyngeal B (parasym)
CN X Vagus B (parasym)
CN XI Spinal Accessory M
CN XII Hypoglossal M
Oh Oh Oh To Touch And Feel Very Good Velvet. Such Heaven
Some Say Marry Money But My Brother Say Big Boobs Matters More
CN I Olfactory
Sensory
Smell
Olfactory cells of nasal mucosa - olfactory bulbs - pyriform cortex
Test: Ask pt if their sense of smell/taste has changed
CN II Optic
Sensory
Function: Vision
Retinal ganglion cells - optic chiasm - thalamus - primary visual cortex in occipital lobe
Test:
Visual Acuity - Snellen Chart
Visual Field and blind spot - move fingers in periphery
Pupillary reflex - Swinging light test, Accomodation
Colour Vision
Fundoscopy - optic disc
Homonymous hemianopia: loss of visual field on same side of both eyes (optic tract, optic radiation, visual cortex - due to aneurym in middle/post cerebral a)
Bitermpral hemianopia: missing outer halves of visual field of both eyes (optic radiation - due to pituitary adenoma, anuerysm in ant/ant communicating a)
CN III Oculomotor
Motor
Nucleus location: midbrain
Movement of eyeball (inferior, superior, medial rectus and inferior oblique) (LR6SO4)
Parasympathetic
Nucleus location: midbrain (Edinger Westphal)
Pupil constriction (cilary muscle, pupillary contrictor muscle)
Oculomotor palsy (decreased/loss of function):
Eye moves down and outwards, ptosis, dilation of pupil
CN IV Trochlear
Motor
Eyeball movement (Superior oblique)
Nucleus location: midbrain (level of inferior colliculus)
Function: depresses adducted eye, intorts (eyes turns in) abdcuted eye
CN II and IV dessucates to contra-lateral side
Trochlear nerve palsy: Diplopia, affected eye will move up causing pt to tilt head (to bring visual fields together)
CN VI Abducens
Motor
Eye movements (Lateral Rectus)
Nucleus: pons
Abducens nerve palsy: Eye turned medially, can’t abduct eye
Internuclear Opthamoplegia:
- Conjugate gaze (movement of both eyes in same direction) palsy
- Lesion in medial longitudinal fasiculus (connects CN III and CN VI)
- Unable to adduct affected eye, and nystagmus of abducted contralateral eye
- Common in MS
Horner’s syndrome
Due to ipsilateral disruption of cervial/thoracic sympathetic chain
Causes: Congenital, Pancoast tumour, MS, Cluster headache
Consists of meiosis, ptosis, anhidrosis, enopthalmos (posterior displacement of eyeball)
CN V Trigeminal
Both
Sensory:
Nucleus location: pons and medulla
Innervates: Face - opthalmic/mandibular/maxillary branches. anterior 2/3 tongue
Motor:
Mastication
Nucleus: pons
Innervates: Masseter, temporalis, medial and lateral and pterygoids
Tests: Sensory: ask pt close eyes, touch forehead, cheek, chin, ask one side feels different)
Motor: ask pt clench teeth and palpate temporalis and masseter
Corneal reflex (afferent: V, efferent: VII)
Herpes Zoster opthalmicus
Reactivation of VZV (singles)
Mostly V1 affected
Elderly, immunocompromised at risk
Treated with oral aciclovir
CN VII Facial
Sensory:
Nucleus: medulla
Function: anterior 2/3 tongue taste
Motor
Nucleus: pons
Function: muscles of facial expression
Parasympathetic
Nucleus: medulla
Salivary/lacrimal glands
Tests:
Ask pt:
Raise eyebrows, Close eyes tightly, blow out cheeks, bare teeth
Corneal reflex: (afferent: V, efferent VII)
Upper and lower motor neuron lesions:
- Bell’s palsy (weakness of facial muscles on one side of face)
Upper: weakens of inf muscles, forehead sparing (due to bilateral innveravation of forehead muscle)
Lower: weakness of sup and inf facial muscles
CN VIII Vestibulocochlear
Sensory
Hearing
Nucleus: pons and medulla
Innervates: Cochlear to autditory cortex in temporal lobes
Balance:
Nucleus: pons and medulla
Innervates: nerve endings in semiciruclar canals - cerebellum and SC
Tests:
Whispering number, ask pt to repeat
Rinne’s (conductive hearing loss), Weber’s (conductive or sensorineural loss)
Describe pathogenesis and clinical presentation of subarachnoid haemorrhage
Definition: Acute cerebrovasuclar event where there is bleeding into the subarachnoid space
Causes:
intracranial aneurysm (bulge in blood vessel due to weakened wall) - most common cause of non-traumatic SA
Other causes: AV malformation, anticoagulants
Risk factors: Marfan syndrome, Ehlers-Danlos Syndrome, polycystic kidney disease
Pathogenesis of SAH
Increased haemodynamic stress leads to inflammatory and immunological reactions - aneurysm formation
Cerebral artery aneurysm ruptures, blood flows in subarachnoid space and ventricles
Clinical presentation:
- Worst headache of their life, nausea/vomiting, photophobia
CN IX Glossopharyngeal
Sensory
Nucleus: medulla
Function: Taste, proprioception for swallowing, BP receptors
Innervates: post. 1/3 tongue, pharyngeal wall, carotid sinuses
Motor: Swallow, gag reflex
Innervates: pharyngeal muscles, lacrimal glands
Parasympathetic: Saliva production
Innervates parotid glands
Tests: Ask pt to cough, use tongue depressor to see palate (soft palate should move up)
Glossopharyngeal palsy:
Uvula moves away from affected side
CN X Vagus
Sensory:
Function: Chemoreceptors, pain receptors (dura) , sensation
Innervates: carotid bodies (BP), respiratory and digestive tracts, pharynx/larynx
Motor:
Function: HR, peristalsis, air flow, speech
Innervates: Heart, smooth muscle of digestive tract, smooth muscles of bronchus, muscles of pharynxlarynx
Parasym:
Innervates smooth msucle and glands as same areas as motor
Tests: Same as glossopharyngeal
CN XI Spinal Accessory
Spinal Acessory
Motor: Trapezius and Sternocleidomastoid
Function: Head rotation, shoulder shrugging
Tests:
- Ask pt to shrug shoulders against your resistance (Trapezius)
- Ask pt to turn head, against your resistance (SCM)
CN VII Hypoglossal
Motor
Function: Speech and swallowing
Tongue
Hypoglossal palsy:
Tongue moves towards lesion
Tests:
Inspect tongue for wasting, fasciculations
Ask pt to move tongue from side to side
CN syndromes
Lesion affected: Jugular foramen
- CN 9, 10, 11
- Paralysis of laryngeal muscles causing voice hoarseness, absent gag reflex, weakness in SCM and trapezius
- Due to tumour
Uvula
Lesion affected: bulbar palsy
CN 9, 10. 11, 12
- Causes dysphagia, difficult in speech, absent gag reflex
- Due to Gullain Barre,
Mononeuropathies: Radial
Entrapment at radial (spiral) groove
Saturday night palsy
Presentation: Wrist and finger drop, painless
Weakness:
Extensor carpi radialis (wrist extension)
Extensor digitorum (finger extension)
Brachioradialis (elbow flexion)
Mononeuropathies: Ulnar
Entrapment at ulnar groove
Presentation: History of elbow trauma, sensory disturbance (4th and 5th digit), painless, weak grip
Weakness:
1st dorsal interosseous (index finger abduction)
Abductor digiti minimi (pinkie abduction)
Flexor carpi ulnaris (wrist flexion)
Adductor policis (thumb adduction)
Mononeuropathies: Median
Entrapment at carpal tunnel
Presentatation: Intermittenet pain during night
- numbness/tingling (first 3 1/2 fingers on palmar surface)
- positive Tinel’s sign (tap on nerve causes pins and needles)
Weakness:
Lumbricals I and II (flexion at MCP joints)
Opponens pollicis (thumb opposition)
Abductor pollicis brevis (abduct thumb)
Flexor pollicis brevis (flex thumb)
Anterior intersosseous branch (of median nerve):
History forearm pain, weak grip, postive Tinel’s sign, cant make OK sign
- pronotor quadtraus (MCP joint flexion)
- flexor digitorum (finger flexion)
- flexor pollicis (thumb flexion)
Mononeuropathies: Common peroneal nerve
L4-S2
Branch of sciatic nerve
Entrapment at fibular head
Presentation:
- History of trauma/surgery/external compression
- Acute onset foot drop, painless,
- Foot inversion not affected (which differentiates it from L5 nerve root neuroapthy)
Weakness:
Tibilas anterior (ankle dorsiflexion)
Extensor hallucis longus (Big toe extension)
Mononeuropathies: femoral nerve
Commonly due to trauma/haemorrhage
Weakness in quads, hip flexion, numbness in medial shin
Weakness:
Quads (extension knee)
Iliopsoas (flexion hip)
Adductor magnus (adduction hip)
Mononeuritis multiplex
Peripheral neuropathy affecting simultaneous or sequential development of 2 or more nerves
Causes:
Diabetes
RA, lupus, sjogren’s syndrome
Sarcoidosis
Hep C/HIV
Lymphoma
What is the peripheral nervous system?
Consists of nerves and ganglia (collection of nerve cell bodies) outside CNS
Allows sensory input to CNS (via dorsal (post) root)
Motor output to muscles (via ventral (ant) root)
Innvervates viscera
Structure:
Bundles of axons in PNS = nerves
Individual axon surrounded by endoneurium
Axon bundled into fascicles and covered by perineurium
Bundle of fascicles covered by epineurium (connective tissue layer)
Nerve Fibre types:
Large myelinated fibres (Motor nerves):
- Proprioception, vibration
Thinly myelinated fibres:
- Light touch, pain, temperation
Unmyelinated fibres:
- Light Touch, pain, temp
Peripheral neuropathy
Damage to peripheral nerves
Presntation depends on which fibres affected:
Motor fibres - weakness
Large fibres - sensory ataxia (due to loss of proprioception), numbness/tingling (loss of light touch), vibration sense,
Small (myelinated/unmyelinated) sensory fibres) - impaired pin prick sensation, temp sensation
Autonomic: postural hypotension, abnormal sweating
Causes: diabetes, hypothyroidism, B12 deficiency
Length dependent axonal neuropathy
Diffuse involvment of peripheral nerves
>50 yrs
Symmetrical
Starts in toes/feet and moves proximally
No significant sensory ataxia
Weakness is distal and mild
Causes:
Diabetes, Alcohol, Nutritional (B12 deficiency), Drugs e.g. Isoniazid, Immune mediated e.g. RA, lupus
Guillain Barre Syndrome
Post-infectious autoimmune neuropathy
Targets myelin sheath
Gradual onset
Medical Emergency
Causes: campylobacter, EBV
- Flaccid, quadraparesis (weakness of all 4 limbs), areflexia (absent reflexes)
+/- Respiratory (e.g. SOB) bulbar duysfunction (e.g. dysphagia), autonomic involvement (tacycardia, HTN)
Treated with IV IG or aphresis
Muscle and Neuromuscular disorders
Clinical features of muscle disorders:
Proximal limb weakness (difficult rasining arms above head, lifting up from seat)
Facial weakness
Eyes: ptosis
Bulbar: dysarthria (difficulty speaking), dysphagia (difficulty swallowing)
Respiratory - breathless esp. when lying flat (as nerves innervating diaphragm isn’t working properly)
Causes of muscle disease:
DMD/BMD
Inflammatory muscle disoders: Polymyositis
NMJ disorders: Myasthenia gravis, Lambert Eaton syndrome
Myasthenia Gravis
Autoimmune disoder where autoantibodies agianst AchR at post-synaptic NMJ.
Decreased generation of muscle APs causing skeletal muscle weakness
Assoc with other autoimmune disorders, and thyoma
Young women, old men
Symptoms:
Fatiguable weakness of ocular, bulbar, respiratory and/or limb muscles
Ptosis, diploplia, dysphagia, dysarthria, proximal muscle weakness
No sensory loss
Investigations:
serum anti-achetylcholine receptor antibodies (AchR) (85% present)
Abnormal single fibre EMG, nerve stimulation
Treatment:
Pyridostigmine (inhibits Ach esterase) and immunosuppressive (steroids, IVIG)
Stroke and TIA
Stroke is defined as an acute neurological deficit lasting more than 24 hours and caused by cerebrovascular aetiology.
Further subdivided into ischaemic stroke (caused by vascular occlusion or stenosis) and haemorrhagic stroke (caused by vascular rupture, resulting in intraparenchymal and/or subarachnoid haemorrhage)
3rd leading cause of death and major cause of disability
Causes: AF, Athersclerosis, AV malformation
Differentials: Migraine, Seizure, Hypoglycaemia, tumour, syncope
Pathophysiology:
- Vessel occlusion due to thrombus from athersclerosis or embolism from carotid a./aorta)
- Reduced cerebral blood flow
- Cell death due to exitoxicity, peri-infart, oxidative stress, depolarisation, inflammation, apoptosis
- Leads to ischaemia (reduced blood flow) and eventually infarction (irreversible damage due to reduced flow)
Transient ischaemic attack (TIA): transient episode of neurological dysfucntion caused by focal ischaemia, without infarction. High risk of ischaemic stroke.
Describe the clinical presentation, investigations and management of stroke / TIA
Clinical presesntation:
Weakness in on side of face/arms/legs (hemiparesis)
Dysphasia (impaired language)
Visual disturbance
Acute light headedness (past-pointing (when pointing at object, will point too far), nystagmus)
Investigations:
FBC, UE, CRP, LFT, lipid profile, glucose, coagulation profile
Glucose, platelet count, coagulation profile may influence acute management
ECG (ischaemic changes, AF)
CT (differentiate between ischaemic/haemorrhagic, exclude tumor)
CT angiogram/MR angiogram (identify site of thrombus, identify ischaemia penumbra - ischaemic tissue that is at risk of infarction but potentially savalgable if reperfusion occurs quickly)
Management:
Ischaemic stroke:
IV thrombolysis (within 4.5 hours) - Alteplase
- NNT: 3.1
Trombectomy (within 6-8 hours) (surgery to remove blood clot)
Aspirin
Admitted to Stroke Unit
Hemicranectomy
Haemorrahagic stroke:
BP control
Admitted to Stroke Unit
Neurosurgical evaluation
Secondary prevention:
Statins, Antiplatelets (clopidorgel or aspirin), antihypertensive e.g. ACEi
Physio, OT, Speech therapy
Risk factors of stroke
Genetics
Poverty
Smoking
Alcohol
Obesity
Hypertension
Common secondary prevention:
Stop smoking, less drinking, lose weight, statins, aspirin
Intracerebral haemorrhage
Defintion: Focal collection of blood in brain parenchyma or ventricular system not due to trauma
Causes:
- Small vessel disease
- Blood clotting disorders
- Tumours
- Drugs e.g. cocaine
Oxfordshire Community Stroke Classification Project
TACS (total anterior circulation syndrome)
- higher cortical dysfunction (dysphasia, visuospatial disturbances), hemiparesis+hemianopia
- MCA (middle cerebral a. or internal carotid a.)
PACS (partial anterior circulation syndrome)
isolated higher cortical dysfunction or 2 of cortical dysfucntion, hemianoipia, hemiparesis
- branch MCA
POCS (posterior circulation syndrome)
- isolated homonymous hemianopia, brainstem syndrome (e.g. nystagmus, cerebellar signs), cranial nerve pasly (ipsilteral) with contralateral motor/sensory defect, bilateral motor/sensory,
- PCA, cerebellar arteries
LACS (lacunar syndrome)
- pure motor (hemiparesis) or sensory stroke or ataxic (lack of voluntary movements) hemiparesis, dysarthria, clumsy hand, mixed sensorimotor
- perforating artery, small vessel disease
The pathophysiological processes that can result in symptoms of stroke
Numbness and weakness in face/arms/legs
Numbness:primary somatosensory cortex becomes damaged
Weakness - primary motor cortex becomes damaged
Ant cerebral a. - motor/sensory symptoms in legs
Middle cerebral a. - symptoms affecting face/upper limbs
Damage to one side will affect body on other side
Dysphasia (difficulty speaking)
Left hemisphere (dominant hemisphere)
Middle cerebral a. supplies Broca’s area (fluid speech production), Wernicke’s area (understanding speech)
Visual disturbances
Posterior cerbral a.
Homonymous hemianopia
Acute lightheadedness
Stroke in cerebellium
(past-pointing (when pointing at object, will point too far), nystagmus)
Describe pathogenesis and clinical presentation of subarachnoid haemorrhage
Definition: Acute cerebrovascular event where there is bleeding into the subarachnoid space and is an emergency
Clinical presentation: Sudden onset headache (worst in their life), nausea/vomiting, loss of consiousness, visual/speech disturbances, seizures
Clinical examination: Photophobia, meningism, vitreous haemorrhage of eye (Terson’s syndrome), speech and limb disturbance
Causes:
Trauma (most common)
Saccular/Berry aneurysms (bulge of intimal layer through muscular wall of a. due to weakened muscular layer of blood vessel wall) - most common cause of non-traumatic SAH
- Most aneursyms at bifurcation of ant. communicating and ant. cerebral a. or ICA and post. communicating a.
- AV malformation, neoplasm, polycystic kidney disease, Ehlers Danlos syndrome
Pathogenesis:
Aneurysm forms due to increased haemodynamic stress which leads to inflammatory and immunlogical reactions and vascular remodelling
Predisposing factors:
Smoking, Female, Hypertension, Ehlers Danlos Syndrome
Graded by WFNS Grades I-V: GCS (lower GCS, higher grade)
Those with non-traumatic SAH, and no aneurysm - perimesencephalic SAH
Discuss the investigation and management of subarachnoid haemorrhage
Investigations:
CT: confirms diagnosis, identifies complications e.g. infarction, hydrocephalus, Fisher Grade used to CT scans for prognosis
Lumbar puncture: xanthochromia (bilirubin in CSF (cerebrospinal fluid)
Once confirmed with CT or LP, causative aneursym can be found using:
CTA (CT angiography - contrast injected to highlight arterial vasculature)
DSA (digital subtraction angiography) - contra-indicated in diabetics, strokes
Hyponatraemia
ECG
Troponin levels
Management:
Bed rest
Fluids - normal saline
Analgeisa
IV Nimodipine: Ca2+ antagonist (prevent vasospams which causes cerebral ischaemia)
Surigcal clipping (close base of aneurysm with a clip)
Endovascular coils (platinum coil inserted into aneurysm, and blodo clot forms around platinum coils which seal aneurysm off.
Complications of subarachnoid haemorrhage
Reharmorrhage (clipping or coiling need to be peformed)
Vasospasm (nimodipine used to prevent it)
Hydrocephalus (accumulation of CSF in brain)
Delayed Ischaemia
Hyponatraemia
Cardiopulmonary complications e.g. arrythmias
Seizures (can be treated with phenytoin)
Predictors of poorer outcome: focal neurological deficit, reduced GCS at presentation, development of complications
Difference between primary headache and secondary headaches syndromes
Primary headache: Headache and assoc. features is primary disorder e.g. migraine, tension, cluster
Secondary headache: Headache is due to underlying disorder e.g. SAH, space-occupying lesion, temporal arteritis, meningitis
Red flags features suggesting secondary headache:
Systemic symptoms e.g. fever, weight loss
Neuroligcal deficit
Onset is acute (thunderclap headache)
Older age onset (>50yrs)
Triggered by posture, valsalva (coughing/straining) - indicates high/low CSF pressure headaches
Thunderclap headache
Definition: sudden onset severe headache, reaches max intensity < 5mins
Considered as SAH until proven otherwise
Site: Occipital
Character:“hit on back of head”
Assoc symptoms:
- Meningismus (photophobia/neck stiffness/headache), vomiting, speech disturbance
Signs:
Positive Kernig’s sign (hip and knee are flexed at 90 degrees, and pain elicited when knee is extended - suggets irritation of meninges)
- Terson’s syndrome, Pulmonary oedema
- IIIrd nerve palsy ( eye down and out, with dilation of pupul - surgical palsy, as parasym fibres which supply pupillary constrictor muscles are compressed from “surgical causes” (from aneurysm - posterior communicating a.). IIrd nerve palsy with no dilation in diabetic pt - ischaemis of small vessels)
Most common non-traumatic cauase: due to berry aneurysms (out pouching of intima through musclar wall)
- Most commonly at anterior cerebral cirulation,. bifurcation of anterior and anterior communicating
- Internal carotid and posteior communicating
at middle cerebral burification
Relevant factors: Usually due to aneurysm, more common in polycystic kidney disease, Ehlers Danlos Syndrome
Risk factors: smoking, alcohol, hypertension
Causes: SAH, intracerebral haemorrhage, bacterial meningitis, primary headache
Investigations
Bloods: FBC, U+Es, LFTs, glucose
ECG - ischaemic changes can be seen
CT - 90% pts will have blood in ventricles (appears white on scan)
LP: xanthochromia (yellow discolouration of CSF due to bilirubin) - only peformed 12 hours after
