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NEUROSURGERY

Terms in this set (383)

- Smoking
- Obesity
- Older age
- Female gender
- Physically strenuous work
- Sedentary work
- Psychologically strenuous work
- Low educational attainment
- Worker's Compensation Insurance
- Job dissatisfaction
- Phsychological factors: somatization disorder, anxiety, and depression

PROGNOSIS OF LOWER BACK PAIN:

- Generally favourable
- 83% had mild or no pain at 1 yr
- 86% had minimal or no disability at 1 yr
-However, only 72% completely recovered
- Psychosocial variables are stronger predictors of long-term disability than anatomic findings on imaging studies

SPONDYLOSIS:

- arthritis of the spin, seen radiographically as disc space narrowing and arthritic changes of the facet joint

SPONDYLOLISTHESIS:

- Anterior displacement of a vertebra on the one beneath it
- A radiologist determines the degree of slippage on spinal X ray
- GRADE I: 1-25% slippage
- GRADE II: 26-50% slippage
- GRADE III: 51-75% slippage
- GRADE IV: 76-100% slippage
- Grade I to II do not require surgical treatment
- Grade III to IV may benefit from surgery

SPINDYLOLYSIS:

- Fracture in the pars interarticularis where the vertebral body and the posterior elements, protecting the nerves are joined
- In a small percent of the adult population, there is a developmental crack in one of the vertebrae, usually at L5

SPINAL STENOSIS:

- Local, segmental, or generalized narrowing of the central spinal canal by bone or soft tissue elements, usually bony hypertrophic changes in the facet joints and by thickening of the ligamentu m flavum

RADICULOPATHY:

- Impairment of a nerve root, usually causing radiating pain, numbness, tingling or muscle weakness that corresponds to a specific nerve root

SCIATICA:

- pain, numbness, tingling in the distribution of the sciatic nerve, radiating down the posterior or lateral aspect of the leg, usually to the foot or ankle

CAUDA EQUINA SYNDROME:

- Loss of bowel of bladder control and numbness in the groin and saddle area of the perineum, associated with weakness of the lower extremities
- Caused by abnormal pressure on the bottom-most portion of the spinal canal and spinal nerve roots, related to either bony stenosis or a large herniated disc

LORDOSIS:

- Inward curve of the lumbar spine
- Excessive = swayback

KYPHOTIC:

- Outward curve of the thoracic spine (at the level of the ribs)
- Too much kyphotic curving causes round shoulders/hunched back. (Scheuermann's disease)

PIRIFORMIS SYNDROME:

- Thought to be a condition in which the piriformis muscle compresses or irritates the sciatic nerve
- The piriformis muscle is a narrow muscle located in the buttocks

DIFFERENTIAL DIAGNOSIS FOR LOW BACK PAIN:

1. MECHANICAL:
- Lumbar strain
- Degenerative disease (discs/facets)
- Spondylolisthesis
- Herniated disc
- Spinal stenosis
- Osteoporosis
- Fractures
- Congenital disease
- Possible spondylolysis
- Facet joint asymmetry
2. NON- MECHANICAL:
- Neoplasia
- Infection
- Inflammatory arthritis
- Scheruermann's disease
- Paget's disease
3. VISCERAL DISEASE:
- Pelvic organs
- Renal disease
- Aortic aneurysm
- Gastrointestinal disease
- Fat herniation

BACK PAIN HISTORY:

- Evidence of systemic disease?
- Evidence of neurologic compromise?
- Social or psychological distress that may contribute to chronic, disabling pain?
- Systemic diagnosis
- Sciatica
- Radiculopathy
- Cauda equina
- Spinal stenosis

UNDERLYING SYSTEMIC DIAGNOSIS:

- History of CANCER
- Age OVER 50
- Unexplained weight loss
- Duration of pain > 1 MONTH
- Nighttime pain
- Unresponsiveness to previous therapies
- IVDU, skin infection, bladder infection or recent fever (spinal infection?)
- < 40 Ankylosing Spondylitis

SCIATICA HISTORY:

- Nerve root irritation typically manifests as sharp or burning pain radiating dow the posterior or lateral aspect of leg, usually into foot or ankle
- Associated numbness or tingling
- Disc herniation: worse with coughing, sneezing, or valsalva maneuver

RADICULOPATHY HISTORY:

- Morst frequent L5 S1 radiculopathy
- PAIN, SENSORY LOSS, WEAKNESS, CHANGE IN REFLEXES

CAUDA EQUINA HISTORY:

- Urinary retention with overflow incontinence
- Saddle anesthesia
- Bilateral sciatica
- Leg weakness
- Caused by tumour pr a massive midline disk herniation
- Medical emergency

SPINAL STENOSIS HISTORY:

- Narrowing of spinal canal, often from bony hypertrophic changes in facet joints and thickening of ligamentum flavum
- Back pain, transient tingling in the legs, ambulation induced pain localized to the calf and distal lower extremity, resolving with rest
- "Neurogenic claudication"
- Relieved by sitting or other spine flexion

PHYSICAL EXAMINATION FOR BACK PAIN:

- INSPECTION OF BACK AND POSTURE: curvature and alignment
- RANGE OF MOTION: flexion and extension, rotation, lateral flexion and extension
- PALPATION: Vertebral tenderness, soft tissue tenderness
- STRAIGHT LEG RAISE: + with sciatica between 10 and 60 degrees
- CROSSED STRAIGHT LEG RAISE: lifting unaffected leg reproduces sciatica in affected leg
- NEUROLOGICAL ASSESSMENT: of L5 and S1 roots
- EVALUATION FOR MALIGNANCY: breast, prostate, lymph nodes
- PERIPHERAL PULSES: r/o vascular claudication
- WADDELL'S SIGNS: inappropriate physical signs

NEUROLOGICAL ASSESSMENT OF L5 AND S1 ROOTS:

- 98% of disc herniations occure at L4-L5 and L5-S1
- L5 MOTOR: angle and great tow dorsiflexion
- L5 SENSORY: numbness medial foot and 1st web space
- S1: ankle reflexes and sensation at posterior calf and lateral foot. Weakness in plantar flexion

WADDELL'S SIGNS:

- Superficial tenderness
- Distracted leg raising
- Non-dermatomal distribution of sensory loss
- Sudden giving way or jerky movements with motor exam
- Inconsistency between spontaneous movements and formal motor testing

L1:

- Inguinal region pain
- Inguinal region sensory loss
- Rare, loss of hip flexion
- No stretch reflex change

L2-L3-L4:

- BACK pain, radiating into ANT THIGH and at times the medial lower leg
- Sensory loss ANT THIGH and occasionally medial lower leg
- Weakness in hip flexion, hip adduction, knee extension
- Loss of patellar tendon reflex

L5:

- BACK pain, radiating to buttock, lateral thigh, lateral calf and dorsum of foot/ Gt toe
- Sensory loss in lateral calf, dorsum of foot, 1st web space
- Weakness in hip abduction, knee flexion, foot dorsiflexion, toe extension, foot inversion and eversion
- Loss of Semitendinosus/semimembranosis (internal hamstrings) tendon reflex

S1:

- Back pain, radiating into buttock, lateral of posterior thigh, posterior calf, lateral or plantar foot
- Sensory loss in posterior calf, lateral or plantar aspect of foot
- Weakness in hip extension, knee flexion, plantar flexion
- Loss of achilles tendon reflex

S2-S3-S4:

- Sacral or buttock pain radiating into the posterior aspect of the leg or the perineum
- Sensory loss medial buttock, perineal, and perianal regions
- WEakness may be minimal; there may be urinary and fecal incontinence or sexual dysfunction
- Loss of bulbocavernosus and anal wink reflexes

APPROACH FOR IMAGING IN BACK PAIN:

- Up to 90% w/o associated symptoms improve rapidly
- Not likely to need imaging in first 4-6 weeks unless neurologic findings or high suspicion of systemic etiology
- Reserve imaging for patients with severe or progressive neurological deficits or serious pathology is suggested in history or physical exam
- If clinical improvement not occurred after 4-6 wk, plain AP and lateral lumbosacral spine useful
- (r/o tumor, infection, instability, spondyloarthropathy, spondylolisthesis)
- CT/MR indicated for progressive neurological deficits, high suspicion of cancer or infection or those with > 12 wks persistent back pain

INDICATIONS FOR REFERRAL:

- Cauda equina syndrome
- Suspected Spinal cord compression (acute neurologic deficits_
- Progressive or severe neurologic deficit

LABORATORY INVESTIGATIONS FOR BACK PAIN:

- ESR/CRP: Infection, malignancy, inflammation
- WBC: infection, inflmmation

RED FLAGS INDICATING RADIOGRAPHIC INVESTIGATION FOR BACK PAIN:

1. Trauma, cumulative trauma
2. Unexplained weight loss
3. Age > 50, especially women, and males with osteoporosis or compression fracture
4. Unexplained fever, history of urinary or other infections
5. Immunosupression or DM
6. History of cancer
7. IV drug use
8. Prolonged use of corticosteroids, osteoporosis
9. Age > 70
10. Focal neurologic deficit with progressive or disabling symptoms, cauda equina syndrome
11. Duration longer than 6 weeks
12. Prior surgery

MANAGEMENT OF ACUTE LOWER BACK PAIN:

1. ACTIVITY MODIFICATION AND BED REST: bed rest no longer recommended. Exercise and resume normal activities ASAP
2. PHARMACOTHERAPY: NSAID or Acetaminophen, Skeletal muscle relaxants (cyclobenzaprine, methocarbamol), opioids, Tramacet, gabapentin
3. ADDITIONAL: manipulation, massage/yoga (+/-), accupuncture/dry needling, cold/hot application, traction/belt/brace

MANAGEMENT OF SUBACUTE/CHRONIC LOW BACK PAIN:

1. PHARMACOLOGIC AND NON-INTERVENTIONAL
2. NON-SURGICAL INTERVENTIONAL
3. SURGICAL

PHARMACOLOGIC AND NON-INTERVENTIONAL TREATMENT OF LOW BACK PAIN:

1. SELF-CARE
2. PHARMACOLOGIC
3. PHYSICAL TREATMENTS
4. PSYCHOLOGICAL/MULTIDISCIPLINARY

SELF-CARE FOR CHRONIC BACK-PAIN:

- maintain activity as tolerated
- education-books, mattress choice (medium firm)
- lumbar support (not proven)

PHARMACOLOGICAL MANAGEMENT OF CHRONIC BACK PAIN:

- Analgesic (tylenol, NSAID 1st line)
- Opioids (short term only)
- Antidepressants (TCA*, not first line. Assess for depression separately.
- Possible benefit from duloxetine)
- Muscle relaxants (adjunctive to analgesics in acute exacerbations)
- Benzodiazepines (short course, acute exacerbations)
- Antiepileptic (Gabapentin, pregabalin, topiramate small unclear effects)
- Anti-TNF-alpha (n role)

PHYSICAL TREATMENTS FOR CHRONIC LOW BACK PAIN:

- Exercise therapy (core, spine mind-body)
- spinal manipulation no advantage to small benefit)
- Acupuncture (unclear, depends on expectations?
- Massage (might be beneficial, esp. in combination with exercise and education)

4.PSYCHOLOGICAL/ MULTIDISCIPLINARY MANAGEMENT FOR CHRONIC LOW BACK PAIN:

- CBT
- COMBINE physical, vocational, behavioural components (intensive interdisciplinary therapy effective)

NON-SURGICAL INTERVENTIONAL TREATMENT OF LOW BACK PAIN:

1. INTERVENTIONAL DIAGNOSTIC PROCEDURES
2. INJECTIONS
3. CHEMONUCLEOLYSIS
4. BOTULINUM TOXIN
5. ELECTROTHERMAL AND RADIOFREQUENCY THERAPIES

INTERVENTIONAL DIAGNOSTIC PROCEDURES FOR CHRONIC LOW BACK PAIN:

- to provoke or temporarily subduue pain
- Used to guide patient selection for interventional treatments or surgery
1. Discograpghy: (+ if reproduces pain)
2. Discoblock: (elimination of pain following LA injection into disc)
3. Nerve root blocks, facet joint blocks, SI joint blocks also used

INJECTIONS FOR LOW BACK PAIN:

1. Epidural glucocorticoid (Short term, mostly in radiculopathy due to herniated disc)
2. Intradiscal injection (no convincing evidence for steroids, Etanercept, or Methylene blue)
3. Local/trigger point injection: no clear evidence. Possibly for tender points elsewhere in the back associated with myofascial pain syndrome
4. Facet joint injection and medial branch block: (no evidence)
5. SI joint injection: (some effect, small trial for SI PAIN)
6. Piriformis syndrome injection: (no trials)

CHEMONUCLEOLYSIS TREATMENT FOR LOW BACK PAIN:

- Treatment of herniated discs with intradiscal injection of enzyme (digesting nucleus pulposus)
- Not as effective as surgery
- Contraindications: spinal stenosis, complete myelographic block, free disc fragments and prior surgery to disc
- Adverse events: Allergic reactions (skin test first), SAH, infection, paraplegia

BOTULINUM TOXIN TREATMENT OF LOW BACK PAIN:

- Paravertebral injection of BotoxA
- Preliminary study: Superior to placebo for 3-4 months

ELECTROTHERMAL AND RADIOFREQUENCY THERAPIES FOR LOW BACK PAIN:

- Intradiscal electrothermal therapy: thermocoagulation of nerves in disc. Not much evidence.
- Radiofrequency denervation: limited evidence

PROLOTHERAPY FOR LOW BACK PAIN:

- repeated injection of irritants into ligaments and tendinous attachments to trigger inflammatory response leading to strengthening of ligaments, decreased pain and decreased disability
- American pain society recommends against

SURGICAL TREATMENT OF CHRONIC LOW BACK PAIN:

- Interbody fusion (suggested for highly selected patient population: non-specific low back pain of degenerative disc disease with presumed discogenic low back pain)
- Artificial disc replacement (suggest not performing)
- Standard open discectomy or microdiscectomy (moderate benefit, suggested, for lumbar disc prolapse with radiculopathy)

INDICATIONS FOR SPINAL SURGERY:

1. URGERNT:
- Severe or progressive motor weakness
- Signs and symptoms of cauda equina
2. ELECTIVE:
- Persistent disabling symptoms impairing quality of life and not responding to non-surgical therapies

NONSPECIFIC LOW BACK PAIN WITH DEGENERATIVE DISC CHANGES:

- Lack of radicular symptoms
- MOST patients with subacute and chronic low back pain
- Not recommended for subacute non-specific back pain
- Few patients report complete symptoms resolution
1. Spinal fusion
2. Lumbar disc replacement

SPINAL FUSION SURGERY:

- Most common surgery for chronic nonspecific low back pain
- Goal is to restrict spinal motion and remove degenerated disc
- Placement of bony graft between vertebrae
- With or without supplemental hardware
- Alters mechanics of spine and is associated with long-term degenerative changes in adjacent segments
- Moderate evidence

LUMBAR DISC REPLACEMENT:

- New alternative to fusion
- Theoretic advantage to preserve ROM and spine mechanics
- Evidence suggests similar efficacy to fusion
- weak evidence

LUMBAR DISC PROLAPSE SURGERY:

- to relieve symptoms due to inflammation of, or pressure on, affected nerve roots by removing part or or the entire disc
- Traditional open discectomy
- Microdiscectomy
- Minimally invasive techniques
- Major post-op complications are rare for any discectomy

SURGERY FOR SPINAL STENOSIS OR SPONDYLOLISTHESIS:

- Degenerative spondylolisthesis caused by degeneration of facets joints and intervertebral discs. A common cause of spinal stenosis
- Leads to loss of normal structural supports, subluxation of vertebral body causing pain and neurological deficit
- Most commonly at L4
- Surgery for pt with persistent symptoms related to spinal stenosis
- Decompressive laminectomy with or without fusions is the most common surgery

SURGERY FOR SPONDYLOLYSIS AND ISTHMIC SPONDYLOLISTHESIS:

- Spondylolysis is a defect in pars interarticularis (the bone connecting one facet joint to another)
- 90% spondylolysis occurs at L5; seen in 6% of adult population. Most are asymptomatic
- Treatment of spondylolysis is controversial; generally not surgical
- Isthmic spondylolisthesis: due to lytic defect, common at L5. Conservative treatment and surgery reserved for non-responders.
- Other indications for surgery: progressive slip, development of neurological deficits, segmental instability associated with pain
- Surgery: posterolateral fusion +/- decompressive laminectomy

SPINAL CORD STIMULATION FOR BACK PAIN:

- For persistent or disabling radicular pain following surgery
- High rate of complications: electrode migration, infection, wound breakdown, generator pocket-related complications, lead problems

DISC ANATOMY:

- Central nucleus pulposus: cushioning
- Surrounded by dense annulus fibrosus
- At birth, nucleus 80% water
- By adulthood, begins to dehydrate and the disc space narrows
- disc space narrowing causes abnormal vertebral stresses and movement, leading to osteogenesis (SPONDYLOSIS)
- Bony growths traumatize nerve roots

DISC HERNIATION:

- Structural failure of disc when nucleus pulposus herniates into spinal canal or neural foramina
- lateral disc herniation causes nerve root compression leading to radicular symptoms
- Central herniation causes myelopathy

HISTORY OF SPONDYLOSIS AND DISC DISEASE:

- Typically older than 50
- Present with PAIN, PARESTHESIAS, or WEAKNESS
- Progressive numbness, weakness and paresthesias in the hands and forearms in a glove like distribution for cervical spondylotic myelopathy
- Patients with radiculopathy secondary to disc disease get pain radiating down arm in nerve root distribution, worsened with neck extension

PHYSICAL EXAM FOR SPONDYLOSIS AND DISC DISEASE:

- Limitation of neck motion
- Straightening of normal cervical lordosis
- Sensory and motor deficits in radicular pattern
- Biceps (C5), brachioradialis (C6), triceps (C7)
- Hyperreflexia and presence of Hoffmann's or Babinski's reflex help determine presence of myelopathy

DIFFERENTIAL DIAGNOSIS OF CERVICAL NECK PAIN:

- Cervical spinal cord or cervical nerve root compresssion
- Rheumatoid arthritis
- Ankylosing spondylitis
- Brachial plexus compression (thoracic outlet syndrome: first or cervical rib and scalenus anticus)
- Peripheral nerve entrapment (carpal tunnel, ulnar nerve palsy) and Pancoast's tumor should be ruled out in patients with arm pain and no neck pain

DIAGNOSTIC EVALUATION FOR NECK PAIN:

- Cervical spine XR: straightening of normal cervical lordosis, disc space narrowing, osteophyte formation, spinal canal narrowing
- Axial diameter of cervical spinal canal < 10 mm= high risk of compression
- CT MYELEOGRAPHY or MRI: evaluate spinal cord and nerve roots
- MRI is study of choice for herniated disc, whereas CT is preferred when bony detail required

TREATMENT FOR CERVICAL NECK PAIN:

1. Medical therapy unless myelopathy or severe radicular weakness
- Cervical traction
- Analgesics
- Muscle relaxants
- More than 95% resolve without surgery
- Procedures that stabilize the spine: anterior cervical fusion
- Decompression laminectomy if diffusely narrow spinal canal and rapidly worsening due to spondylotic myelopathy

PRESENTATION OF LUMBAR DISC DISEASE:

- COMMON
- PAIN radiating down lower extremity

PHYSICAL EXAM FOR LUMBAR DISC DISEASE:

- SCIATICA caused by disc herniation and compression of nerve root, leading to radicular pain
- L4-L5 and L5-S1 most commonly prolapsed leading to L5 and S1 nerve root symptoms
- Paresthesia, numbness and weakness
- Straight leg raise: ispilateral and contralateral
- Absence of ankle or knee reflex, weakness of foot dorsiflexion or plantar flexion or weakness of knee extension

DIAGNOSIS OF LUMBAR DISC DISEASE:

- Clinical diagnosis confirmed by MRI demonstrating disc protrusion

TREATMENT OF LUMBAR DISC DISEASE:

- Most improve without surgery
- One indication for surgery is chronic disabling intractable pain
- Open laminectomy and discectomy
- Urgent surgery if progressive neurological deficit, acute onset cauda equina syndrome

NEURO SCREEN:

1. LOOK
2. MOTOR
3. SENSORY
4. REFLEXES
5. MUSCLE TONE

NEURO INSPECTION:

- Facial symmetry, pupil size (Horner's syndrome)
- Muscle atrophy: Shoulder and hip girdle and hands
- Fasciculations in hands, legs

MOTOR MYOTOMES:

- C5= DELTOID (Axillary)
- C5/C6= BICEPS (Musculocutaneous)
- C6 = WRIST EXTENSORS (Radial)
- C7= TRICEPS (Radial and Axillary)
- C8= DEEP FINGER FLEXORS (Median and Ulnar)
- T1= FINGER ABDUCTORS (dorsal interossei) (Ulnar)
- L2/L3= HIP FLEXORS (Iliopsoas) (Femoral)
- L3/L4= KNEE EXTENSION (quadriceps) (Femoral)
- L4= TIBIALIS ANTERIOR (Deep fibular nerve)
- L5= EXTENSOR HALLUCIS LONGUS (Deep fibular)
- S1/S2= GASTROC-SOLEUS (Tibial)

GRADING MUSCLE STRENGTH:

(0 = no voluntary movement
1 = flicker of movement
2 full range with gravity eliminated
3 full range against gravity
4 full range but cannot overcome resistance)
5 = full range against resistance

UPPER EXTREMITY DERMATOMES:

- C2= Occiput
- C3= Supraclavicular fossa
- C4 = posterior shoulder
- C5= Anterior deltoid and biceps
- C6= Radial forearm
- C7= 2nd and 3rd digits
- C8= 4th and 5th digits
- T1= Ulnar forearms
- T2= Medial upper arm

LOWER EXTREMITY DERMATOMES:

- L1= Inguinal ligament
- L2= Anterior upper thigh
- L3= Knee
- L4= Medial lower leg
- L5= first web space
- S1= Lateral border of the foot and heel

UPPER EXTREMITY PERIPHERAL NERVES:

- Axillary= Deltoid area
- Lateral cutaneous nerve of forearm=Lateral forearm
- Medial cutaneous nerve of forearm= medial forearm
- Median Nerve= thumb
- Ulnar nerve= little finger
- Radial nerve= dorsum of the hand

LOWER EXTREMITY PERIPHERAL NERVES:

- Femoral cutaneous nerve= anterior thigh
- Obturator nerve= Medial thigh
- Lateral cutaneous nerve of calf= lateral calf
- Saphenous nerve= Medial calf
- Sural nerve= Lateral foot
- Deep peroneal nerve= 1st web space
- Superficial peroneal nerve= Dorsum of foot
- Plantar nerves= sole, medial and lateral

REFLEXES:

➢ (graded 0-4+)
- Biceps (C5)
- Brachioradialis (C6)
- Triceps (C7)
- Patellar tendon (L2,L3)
- Achilles Tendon (S1-S2)

MUSCLE TONE:

- Quick passive movement of elbow, wrist, knee and ankle

MENTAL STATUS TESTING:

- LEVEL OF CONSCIUSNESS: drowsiness, coma, alert
- ORIENTATION: year, season, date, day, month
- ATTENTION AND MEMORY: name 3 words, serial sevens, recall 3 words
- LANGUAGE: Name objects, No ifs ands or buts, take paper in right hand, fold it in half, and put it on the floor, read this and do what it says, Write a sentence
- SPATIAL ORIENTATION: touching pentagons

CRANIAL NERVE TESTING:

o Ask about smell. (I)
o Visual acuity, confrontational fields, eye movements, saccades, accommodation, convergence, pupils' response to light, swinging light test, fundoscopy. (II, III, IV, VI)
o Facial sensation, muscles of mastication (biting down and feeling for masseter and temporalis, side-side + in-out movements of jaw for pterygoids). (V)
o Facial strength: wrinkle forehead, close eyes tightly, show teeth, puff out cheeks, blow out a candle, say "me, me, me, me, me", corneal reflex. (VII)
o Hearing: rub fingers near ears, Rinne and Weber tests w/256 Hz fork. (VIII)
o Palatal movement, gag reflex. (IX, X)
o Side-side head rotation against force, shoulder elevation. (XI)
o Tongue in bottom of mouth, movement, strength in cheek, say "t,t,t,t,t,t". (XII)

UPPER LIMB NEURO EXAM:

o Inspect: atrophy, involuntary movements, scars
o Tone: rate dependant, test biceps, triceps, wrist flex/exten/supin/prona
o Power: shoulder abduction, elbow flexion/extension, wrist flexion/extension, finger flexion/extension/abduction, pronator drift
o Sensation: initially run tissue distal→proximal to see if any peripheral neuropathy
• Light touch, Pain/Temp, Vibration (128 Hz) on joint, Joint proprioception x5, Graphesthesias for cortical sensation on palmar surface
o Cerebellar function: fine finger movements, rapid alternating movements in one spot, hand-rolling, finger to nose
o Reflexes: Biceps C5, Brachioradialis C6, Triceps C7

LOWER LIMB NEURO EXAM:

o Inspect: atrophy, involuntary movements, scars
o Tone: test hip flexors, knee flexors/extensors
o Power: hip flexion/extension, knee flexion/extension, ankle dorsiflexion/plantar flexion
o Sensation: initially run tissue distal→proximal to see if any peripheral neuropathy
• Light touch, Pain/Temp, Vibration (128 Hz) on joint, Joint proprioception x5, Graphesthesias for cortical sensation dorsum of foot
o Cerebellar function: heel-to-knee tap x3 then run heel down shin to big toe
o Reflexes: Patellar L3/L4, Achilles S1, Plantar response

ANEURYSMS OF THE CIRCLE OF WILLIS

1. ACOM: 30%
2. INTERNAL CAROTID/PCOM: 30%
3. MCA: 20%
4. BASILAR TIP: 7%
5. SUPERIOR CEREBELLAR: 3%
6.PICA: 3%
7. VERTEBROBASILAR: 2%

ACA SUPPLIES:

- Midline/medial portions, frontal, parietal lobes

MCA SUPPLIES:

- Lateral cerebral cortex (frontal, temporal, and parietal)
- Anterior temporal lobes
- Insular cortices
- M1: lenticulostriate to basal ganglia/internal capsule
- M2: Insular

BASILAR ARTERY SUPPLIES:

- Pons

AICA SUPPLIES:

- Mid level cerebellum

PICA SUPPLIES:

- Inferior cerebellum

VERTEBRAL ARTERY SUPPLIES:

- Lateral medulla (olives)

SUPERIOR CEREBELLAR ARTERY SUPPLIES:

- Superior cerebellum

ANTERIOR CHOROIDAL ARTERY SUPPLIES:

- Thalamus and hypothalamus

ANTERIOR SPINAL ARTERY SUPPLIES:

- Anterior medulla
- Anterior 2/3 or cord

POSTERIOR SPINAL ARTERY SUPPLIES:

- Posterior medulla
- Posterior 1/3 or cord

INTRACRANIAL MASS LESION DIFFERENTIAL:

1. Tumour
2. Pus/Inlammation
3. Blood
4. Cyst

BRAIN TUMOUR DIFFERENTIAL:

- Metastatic
- Astrocytoma
- Meningioma
- Vestibular schwannoma (acoustic neuroma)
- Pituitary adenoma
- Primary CNS lymphoma

INFLAMMATORY BRAIN MASSES:

- Cerebral abscess
- Extradural abscess
- Subdural empyema
- Encephalitis
- Tumefative MS

BLOOD BRAIN MASSES:

- Extradural (epidural) hematoma
- Subdural hematoma
- Ischemic stroke
- Hemorrhage: SAH, ICH, IVH

CLASSIFICATION OF SPINE DISORDERS:

- Extradural
- Intradural extramedullary
- Intradural intramedullary

EXTRADURAL SPINE DISORDERS:

- Degenerative: disc herniation, canal stenosis, spondylolisthesis, spondylolysis
- Infection/inflammation: osteomyelitis, discitis
- Ligamentous: ossification of posterior longitudinal ligament
- Trauma: mechanical compression, instability, hematoma
- Tumours: lymphoma, metastatic (lymphoma, lung, breast, prostate), neurofibroma

INTRADURAL EXTRAMEDULLARY SPINE DISORDERS:

- Vascular: dural Arterio-venous fistula, subdural hematoma
- Tumours: meningioma, schwannoma, neurofibroma

INTRAMEDULLARY SPINE DISORDERS:

- Tumors (rare): astrocytoma, ependymoma, hemangioblastoma, dermoid
- Syringomyelia (trauma, congenital, idiopathic)
- Infectious/inflmmatory: TB, sarcoid, transverse myelitis
- vascular: AVM, Ischemia

PERIPHERAL NERVE LESIONS:

- Traumatic
- Entrapment
- Iatrogenic
- Inflammatory
- Tumours

ICP/VOLUME RELATIONSHIP:

- Adult skill is rigid, constant intracranial volume
- Increase in one constituent = inc ICP
- ICP does not rise initially due to autoregulation
1. IMMEDIATE COMPENSATION: displacement of CSF to lumbar theca, displacement of blood from sinuses
2. DELAYED COMPENSATION: displacement of ECF or ICF; displacement of brain tissue
- When ICP is exhausted, ICP rises exponentially

MONRO-KELLIE DOCTERINE:

- Vbrain + Vblood + Vcsf + Vlesion
= Vskull
= Contant

CEREBRAL BLOOD FLOW:

- Dependent on CPP and CVR
- CBF = CPP/CVR
- Normal CPP is > 50 mmHg in adults
- Cerebral autoregulation maintains CBF by compensating for changes in CPP
- CPP = MAP - ICP
- Autoregulation fails if CPP < 60 due to ICP, MAP > 150, MAP <50, or in brain injury

ICP MEASUREMENT:

- Noraml ICP < 15 mmHg adult, 3-7 mmHg child
- Varies with patient position
- moderate elevation ICP > 20
- Severe elevation ICP > 40
- Traube-Herine waves: respiratory and cardiac pulsations
- Plateau wave: ICP over 50 mmHg, 5-20 min precedes further deterioration

ACUTE MONITORING OF ICP:

- Lumbar puncture (contraindicated with known or suspected intracranial mass)
- Intraventricular catheter/ventriculostomy/external ventricular vein
- (also therapeutic)

CHRONIC MONITORING OF ICP:

= Fibreoptic monitoring (intraventricular, intraparenchymal, subdural), subarachnoid bolt, epidural monitor

WHEN TO MONITOR ICP:

1. Pt with abnormal head CT and GCS 3-8 after cardiopulmonary resuscitation
2. Pt normal head CT, GCS 3-8 and two or more of: age > 40, uni or bilateral motor posturing, systolic BP < 90 mmHg
3. Postoperative monitoring
4. Investigation of normal pressure hydrocephalus (NPH)

CAUSES OF ELEVATED ICP:

1. Space occupying lesion: tumor, pus, blood, skull fracture, foreign body
2. Intracranial blood volume: vasodilatation (inc PCO2, dec PO2, dec pH = HYPOVENTILATION), venous outflow obstruction
3. Cerebral edema (vasogenic, cytotoxic, osmotic)
4. Impaired autoregulation (hypotension, hypertension, brain injury)
5. Hydrocephalus
6. Tension pneumocephalus
7. Pseudotumor cerebri
8. Status epilepticus

CLINICAL FEATURES OF ACUTE ELEVATION IN ICP:

- Headache: worse in am, aggrevating by stoop,bend
- NV
- Decreased LOC: ICP + DBP or midbrain compression
- Drop in GCS: best index of progress
- Papilledema +/- retinal hemorrhages (24-48hr)
- Abnormal extraoccular eye movements: CNVI palsy, Upward gaze palsy
- Herniation syndrome
- Focal signs and symptoms

CUSHING'S TRIAD:

- Acute raise in ICP; full triad in 33%
1. Hypertension
2. Bradycardia (late)
3. Irregular respiratory pattern

CLINICAL PRESENTATION OF CHRONIC ELEVATION IN ICP:

- Headache: worse with cough, strain, bend and worse in morning and evening (vasodilatation due to increased CO2 with recumbency
- VISUAL CHANGES: due to papilledema, enlarged blind spot, optic atrophy/blindness
- Decreased LOC

INVESTIGATIONS OF ELEVATED ICP:

- Urget CT/MR
- ICP monitoring may be appropriate

HERNIATION SYNDROMES:

1. SUBFALCINE
2. CENTRAL TENTORIAL (AXIAL)
3. LATERAL TENTORIAL (UNCAL)
4. UPWARD
5. TOSILLAR

SUBFALCINE HERNIATION:

- Cingulate gyrus herniates under falx cerbri
- Caused by lateral supratentorial lesion
- Usually asymptomatic
- Warns of impending transtentorial herniation
- Risk ACA compression

CENTRAL TENTORIAL (AXIAL) HERNIATION:

- Displacement of diencephalon through tentorial notch
- Caused by supratentorial midline lesion, diffuse cerebral swelling, late uncal herniation
- Small pupils, moderately dilated, fixed
- Decreased LOC (midbrain)
- EOM/Upward gaze impairment: pretectum and superior colliculi
- Brainstem hemorrhage
- Diabetes insipidus (pit stalk and hypothalamus)

LATERAL TENTORIAL HERNIATION (UNCAL):

- Uncus of temporal lobe herniates down through tentorial notch
- Caused by lateral supratentorial lesion (often rapidly expanding traumatic hematoma)
- Ispilateral non-reactive dilated pupil
- ipsilateral EOM paralysis, ptosis
- Decreased LOC
- Contralateral hemiplegia (cerebral peduncle)

UPWARD HERNIATION:

- Cerebellar vermis herniates through tentorial incisura
- Large posterior fossa mass
- Cerebellar infarct
- hydrocephalus from compression of cerebral aqueduct

TONSILLAR HERNIATION:

- Cerebellar tonsils herniate through foramen magnum
- Caused by infratentorial lesion, following central tentorial herniation, or following LP in presence of intracranial mass lesion
- Neck stiffness and head tilt
- Decreased LOC
- Flaccid paralysis
- Respiratory irregularity
- Blood pressure instability

TREATMENT OF ELEVATED ICP:

- CT / MR to identify etiology, assess midline shift and herniation
- Treat primary cause (remove mass, ventilate)
- If ICP persists, treat when ICP > 20
- Keep ICP < 20, CPP > 65, MA > 90
1. CONSERVATIVE:
2. AGGRESSIVE:
- ICP HEAD
- I: Intubate
- C: Calm / Coma
- P: place drain/paralysis
- H: Hyperventilate
- E: elevate head
- A: Adequate BP (>90)
- D: diuretic (mannitol)

CONSERVATIVE ICP INTERVENTION:

- Elevate head of bed to 30 (inc venous outflow)
- Prevent hypotension with fluid and vasopressors, dopamine, norepinephrine PRN
- Ventilate to normocarbia (35-40)
- Oxygen to maintain PO2 . 60
- Osmolar diuresis: mannitl 20% IV 1-1.5 g/kg then .25 g/kg q6h so serum 315-320
- Corticosteroid (delayed) for tumour, abscess, blood

AGGRESSIVE ICP INTERVENTION:

- Sedation (light barbituate/codiene to heavy fentanyl/MgSO4)
- Paralysis (vecuronium)
- Hyperventilate 30-35
- Drain 3-5 mL CSF
- Inserve EVD or shunt
- Coma (pentobarbital)
- Decompressive craniotomy
- No role for hypothermia in head injury

HYDROCEPHALUS:

- Increase in CSF volume
- Caused by obstruction to flow, decreased CSF absorption, Increased CSF prouction (rare)
- 1-1.5% incidence
- Congenital hydrocephalus 1-2/1000 live births

CLASSIFICATION OF HYDROCEPHALUS:

1. Obstructive (non-communiating) hydrocephalus
2. Non-obstructive (communicating) hydrocephalus)
3. Normal pressure hydrocephalus
4. Hydrocephalus ex vacuo

OBSTRUCTIVE HYDROCEPHALUS:

- Circulation blocked within ventricular system proximal to arachnoid granulations
1. ACQUIRED: aqueductal stenosis, intraventricular lesion, Tentorial herniation, neurosarcoidosis, abscess, granuloma, arachnoid cyst
2. CONGENITAL: Aqueductal stenosis, dandy-walker malformation, Chiari malformation
> FINDINGS:
- Ventricular enlargement proximal to block
- Periventricular hypodensity (transependymal migration of CSF)
- Sulcal effacement

NON-OBSTRUCTIVE HYDROCEPHALUS:

- CSF absorption blocked at extraventricular site = arachnoid granulations
1. Post infectious (common): meningitis, cysticercosis
2. Post-hemorrhagic (2nd): SAH, IVH, trauma
3. Choroid plexus papilloma
4. idiopathic
- ALL VENTRICLES DILATED

NORMAL PRESSURE HYDROCEPHALUS:

- Persistent ventricular dilatation in the context of normal CSF pressure
- idiopathic 50%
- SAH, meningitis, trauma, radiation induced
> FINDINGS:
- Enlarged ventricles without increased prominence of cerebral sulci

HYDROCEPHALUS EX VACUO:

- Ventricular enlargement resulting from atrophy of surrounding brain tissue
- Caused by aging, alzheimers, CJD
- Enlarged ventricles and sulci
- Cerebral atrophy

CSF PRODUCTION:

- Produced by choroid plexus in lateral ventricles
- Production = reabsorption
- 500 mL /d
-Normal CSF volume is 150 mL

FLOW OF CSF:

1. Lateral ventricles
2. Choroid plexus
3. Third ventricle
4. Cerebral aqueduct (Sylvius)
5. Fourth ventricle
6. Foramina of Luschka and Magendie
7. Arachnoid granulations
8. Subarachnoid space
9. Superior sagittal sinus

CLINICAL FEATURES OF HYDROCEPHALUS:

1. ACUTE: SSx of elevated ICP (impaired upward gaze, CN VI palsy)
2. CHRONIC/GRADUAL ONSET HYDROCEPHALUS (NPH): ataxia, apraxia, urinary incontinence, dementia (CLASSIC TRIAD OF NPH)

INVESTIGATIONS FOR HYDROCEPHALUS:

- CT/MRI
- US through anterior fontanelle in infants
- ICP monitoring to investigate PH or test response to shunting
- Radionucllide cisternography can test CSF flow and asborptionrate
- B-2 transferrin assay to test for CSF leak

TREATMENT OF HYDROCEPHALUS:

- Ventricular drainage
- Surgical removal of obstruction
- Excision of choroidal papilloma
- SHUNT: VP, ventriculopleural, Ventriculoatrial, lumboperitoneal
- Third ventriculostomy
- LPs

SHUNT COMPLICATIONS:

1. Obstruction
2. Infection(3-6%)
3. Overshunting (10% over 6.5 yr)
4. Seizures (5%)
5. Inguinal hernias (17% VP infant)

IDIOPATHIC INTRACRANIAL HYPERTENSION:

- PSEUDOTUMOR CEREBRI
- Raised ICP and papilledema without evidence of mass lesion, hydrocephalus or hypertensive encephalopathy
- "diagnosis of exclusion"
- Etx unknown
- Associated with lateral venous sinus thrombosis, Obesity, hypervitaminosis A, Endocrine abnormalities, iron deficiency anemia, polycythemia vera, steroids, tetracycline
- Similar risk factors to gall stones: fat, female, fertile, forties = venous sinus thrombosis

CLINICAL FEATURES OF IDIOPATHIC INTRACRANIAL HYPERTENSION:

- SSx of raised ICP (Headache > 90%, pulsatile intracranial noise, no LOC, no diplopia)
- Decreased visual acuity, papilledema, visual field defect, optic atrophy
- usually self-limited, recurrence is common, chronic in some patients
- Risk of blindness not correlated to SSx or clinical course

INVESTIGATIONS FOR IDIOPATHIC INTRACRANIAL HYPERTENSION:

- CT: Normal
- CSF: normal
- MRI: look for venous sinus thrombosis

TREATMENT OF IDIOPATHIC INTRACRANIAL HYPERTENSION:

- R/O true intracranial hypertension (sinus thrombosis)
- Discontinue offending medications, encourage weightloss, fluid/salt restriction
- Pharmacotherapy: acetazolamide, thiazide diuretic, furosemide
- Serial LP or shunt
- Optic nerve sheath decompression
- 2 yr follow up with imaging to r/o tumor
- Ophthamology f/u

IMPORTANT FEATURES OF HEAD CT/MR:

- lesions (+/- edea, necrosis, hemorrhage)
- Midline shifts and herniations
- Effacement of ventricles and sulci, basal cisterns
- Single or multiple (metastatic)

BRAIN TUMOR LOCATIONS:

- VENTRICULAR
- SUPRATENTORIAL EXTRA AXIAL
- SUPRATENTORIAL INTRA-AXIAL
- SKULL BASE
- SELLAR OR SUPRASELLAR
- POSTERIOR FOSSA-EXTRA AXIAL
- POSTERIOR FOSSA- INTRA AXIAL

VENTRICULAR TUMORS:

- colloid cyst
- Choroid plexus papilloma
- Ependymoma
- Germinoma
- Teratoma
- Menignioma

SUPRATENTORIAL EXTRA-AXIAL TUMOURS:

- Meningioma
- Cyst

SUPRATENTORIAL INTRA-AXIAL TUMOURS:

- astrocytoma
- Glioblastoma
- Oligodendroglioma
- Ganglioma
- Lymphoma
- Metastases

SKULL BASES TUMORS:

- Carcinoma
- Chordoma
- Glomus jugulare
- Osteoma

SELLAR AND SUPRASELLA TUMORS:

- Pituitary adenoma
- Craniopharyngioma
- Optic nerve glioma
- Cyst

POSTERIOR FOSSA INTRA-AXIAL TUMORS

- Schwannoma
- meningioma
- Cysts
- Metastases

POSTERIOR FOSSA EXTRA-AXIAL:

- Schwannoma, menignioma, cyst, metastases

DDx FOR RING ENHANCING LESION ON CONTRAST CT:

- MAGICAL DR
- M: Metastases
- A: Abscess
- G: Glioblastoma (high grade astrocytoma)
- I: Infarct
- C: Contusion
- A: AIDS (Toxoplasmosis)
- D: Demyelination
- R: Resolving hematoma

PRIMARY SOURCES OF METASTATIC BRAIN TUMOURS:

- Lung: 44%
- Breast: 10%
- Kidney (RCC): 7%
- GI: 6%
- Melanoma: 3%

BENIGN BRAIN TUMOURS:

- non-invasive
- Devastating due to expansion of mass in fixed volume of skull (mass effect)

MALIGNANT BRAIN TUMOURS:

- Implies rapid growth, invasiveness but extracranial metastasis

METASTATIC BRAIN TUMOURS:

- Most common brain tumour seen clinically
- 15-20% of cancer pt present with cerebral metastatic tumours
- Most common: LUNG BREAST
- Other: kidney, thyroid, stomach, prostate, testis, melanoma
- Usually by hematogenous spread
- 80% are hemispheric, often at grey-white matter junction or junction or temporal-parietal-occipital lobes

INVESTIGATIONS FOR BRAIN METS:

- Identify primary tumour: Metastatic workup (CXR, CT chest/abdo/pelvis, Abdo US, Bone scan, Mammogram)
- CT with contrast (round, well circumscribed, ring enhancing, ++ edema, often multiple
- MRI more sensitive, especially for posterior fossa
- Consider biopsy in unusual cases or if no primary found

TREATMENT OF BRAIN METS:

1. MEDICAL
- Phenytoin for seizure prophylaxis
- Dexamethasone to reduce edema givin with ranitidine
- Chemotherapy
2. RADIATION:
- Stereotactic radiosurgery: discrete, deep seated inoperable tumours
- Multiple lesionsL use whole brain radiation therapy
- Post-op whole brain radiation common
3. SURGICAL:
- Single/solitary lesions: surgery + radiation

PROGNOSIS OF BRAIN METS:

- Median survival without treatment once symptomatic is 1 months
- WIth optimal treatment is 6-9 months

ASTROCYTOMA:

- Most common primary intra-axial brain tumour, common 4-6th decades
- Sites: cerebral hemispheres>>>cerebellum, brainstem, spinal cord
- Symptoms: recent onset of new/worsening HA, NV, seizure, focal deficits or signs of increased ICP

GRADING OF ASTROCYTOMA:

- I: Pilocytic astrocytoma (mass effect, enhancement on CT/MR) > 10 yr survival and cure if total resection
- II: Low grade/diffuse (mass effect, no enhancement) 5 year survival
- III: Anaplastic (complex enhancement) 1.5-2yr survival
- IV: Glioblastoma multiforme (GBM) (Necrosis, ring enhancement) 12 months, 10% 2 yr

CT FEATURES OF HIGH GRADE ASTROCYTOMA:

- Heterogenous contrast enhancement
- Ill-defined borders (infiltrative)
- Peritumoural edema
- Central necrosis
- Compression of ventricles

INVESTIGATIONS FOR ASTROCYTOMA:

- CT/MRI WITH CONTRAST
- Tissue biopsy: WHO grade and histology correlates with prognosis, but 25% sampling error

TREATMENT OF ASTROCYTOMA:

1. LOW GRADE
- Close follow up, radiation, chemo, surgery
- Surgery is non-curative
- Radiation prolongs survival
- Chemo reserved for tumour progression
2. HIGH GRADE ASTROCYTOMA:
- Surgery: gross total resection as allowed
- Stereotactic biopsy
- Expectant
- Prolong "quality" survival
- Chemotherapy: 20% response,
- Multiple gliomas: Whole brain radiation therapy +/- chemotherapy

MENINGIOMA:

- Mostly benign (1-2% anaplastic), slow-growing, extra-axial, circumscribed (non-infiltrative), arise from arachnoid membrane
- Often calcified and hyperostosis of adjacent bone
- Classically Psammoma bodies on histology
- Location: parasagittal convexity or falx (70%), sphenoid wing, tuberculum sellae, foramen magnum, olfactory groove

CLINICAL FEATURES OF MENINGIOMA:

- Middle aged
- Female 3:2
- High progesterone receptors
- Symptoms of increased ICP
- Focal deficit
- Usually solitary
- 10% multiple (loss of NF2 gene/22q12 deletion)

INVESTIGATIONS FOR MENIGNIOMA:

- CT with contrast
- Contrast enhanced MRI
- Angiography: most supplied by external carotid feeders, assess venous sinus involvement (tumour blush)
- Octreotide scintigraphy: expression of somatostatin receptor

CT FEATURES OF MENINGIOMA:

- Homogenous dense contrast enhancement
- dural attachment
- Distinct margins, well-circumscribed

TREATMENT OF MENINGIOMA:

- Conservative management for non-progressive, asymptomatic lesions
- Surgery is treatment of choice if symptomatic or progression on sequential imaging (complete resection is cure)
- Stereotactic radiosurgery for lesions < 3 cm
- Endovascular embolization to facilitate surgery
- Radiation for recurrent, atypical, malignant
- > 90% 5 year survival, 10-20% recurrence
- Depends on extend of resection

WHO CLASSIFICATION OF MENINGIOMA:

- Grade 1: low risk of recurrence
- Grade 2: intermediate risk of recurrence
- Grade 3: High risk of recurrence
- Based on histology

VESTIBULAR SCHWANNOMA:

- Acoustic neuroma
- Slow growing, avg. 1 mm / yr
- benign posterior fossa tumour
- Arises from vestibular component of CN VIII in internal auditory canal, expanding into bony canal and cerebello-pontine angle (CPA)
- If bilateral, diagnostic of Neurofibromatosis type II
- peak age 4-6th decade

CLINICAL FEATURES OF VESTIBULAR SCHWANNOMA:

- Compression of CPA structures
- CN VIII compression (hearing loss 98%, tinnitus, dysequilibrium)
- later CN V and CN VII compression
- Ataxia and raised ICP late

INVESTIGATIONS FOR VESTIBULAR SCHWANNOMA:

- MRI with gadolinium, or T2 fiesta sequence
- CT with contrast second choice
- Audiogram, brainstem auditory evoked potentials, caloric testing

TREATMENT OF VESTIBULAR SCHWANNOMA:

- Conserviate: serial imaging
- Radiation: stereotactic radiosurgery or fractionated radiotherapy
- Surgery if: lesion < 3cm, brainstem compression, edema, hydrocephalus
- Curable if complete resection, but almost always impossible
- Operative complications: CN VII, CN VIII, CSF leak

PITUITARY ADENOMA:

- Primarily anterior pit, 3rd-4th decades, M = F
- Incidence in autopsy 20%
- Classification: micro<1cm, macro > 1
- Functional/secretory vs inactive
- Differential diagnosis: Parasellar tumours (Craniopharyngioma, teberculum sellae meningioma), carotid aneursym

CLINICAL FEATURES OF PITUITARY ADENOMA:

- MASS EFFECTS: HA, Bitemporal hemianopsia, CN III, IV, V1, V2, VI palsy
- ENDOCRINE:
1. Prolactin: infertility, amenorrhea, galactorrhea, decreased libido
2. ACTH: Cushing's, hyperpigmentation
3. GH: acromegaly/giagantism
4. Panhypopit:(hypothryoid, adrenalism, gonadism)
5. MEN 1 syndrome
6. Diabetes insiipidus
- PITUITARY APOPLEXY: sudden expansion of mass due to hemorrhage or necrosis. Abrupt onset HA, visual change, ophthalmoplegia, reduced mental status, panhypopit

COMPRESSIVE ADENOMA ENDOCRINE CHANGES:

- Go Look For The Adenoma Please
- GH, LH, FSH, TSH, ACTH, Prolactin affected in this order

INVESTIGATIONS OF PITUITARY ADENOMA:

- Formal visual fields
- CN testing
- Endocrine tests (Prolactin, TSH, AM cortisol, fasting glucose, FSH/LH, IGF-1), electrolytes, urine analysis/osmolarity
- Imaging: MRI with and without contrast

TREATMENT OF PITUITARY ADENOMA:

1. MEDICAL:
- For apoplexy (rapid corticosteroid +/- surgical decompression)
- Bromocriptine (Dopamine agonist) for Prolactinoma
- Cushing's: serotonin antagonist, inhibit cortisol production (ketokonazole)
- Acromegaly: somatostatin analogue (octreotide) +/- bromocriptine
- Endocrine replacement therapy
2. SURGICAL:
- Trans-sphenoidal, trans-ethmoidal, trans-cranial approaches for non-secreting adenomas causing mass effect and Cushing/Acromegaly (50% cure rate)

4 ROUTES OF MICROBIAL ACCESS TO CNS:

1. HEMATOGENOUS
2. DIRECT
3. CONTIGUOUS SPREAD
4. SPREAD FROM PNS

HEMATOGENOUS SPREAD TO CNS:

- Most common
- arterial and retrograde venous
- Adults: chest is #1 source (lung abscess, bronchiectasis, empyema)
- Children: congenital cyanotic heart disease with R to L shunt
- Immunosuppression (AIDS-toxoplasmosis)

DIRECT IMPLANTATION OF INFECTION TO CNS:

- Dural disruption
- Trauma
- Iatrogenic (LP, post-op)
- Congenial defect (dermal sinus)

CONTIGUOUS SPREAD TO CNS:

- Adjacent infection
- From air sinus, naso/oropharynx, surgical site (otitis media, mastoiditis, sinusitis, osteomyelitis, dental abscess)

SPREAD FROM PNS TO CNS:

- Virus: rabies, herpes zoster

COMMON EXAMPLES OF PUS AND INFLAMMATION IN THE BRAIN:

1. Epidural abscess: in cranial and spinal epidural space, associated with osteomyelitis. Treat w/ drainage and Abx, surgical emergency if cord compression
2. SUBDURAL EMPYEMA: bacterial/fungal infection, due to contiguous spread from bone or air sinus, progresses rapidly. Treat w/ surgical drainage and Abx (20% mortality)
3. MENINGITIS, ENCEPHALITIS
4. CEREBRAL ABSCESS

CEREBRAL ABSCESS:

- Pus in brain substance, surrounded by tissue reaction (capsule formation)
- Pathogenesis:
1. Streptococcus (most common)
2. Staphylococcus (penetrating)
3. Gram negatives, anaerobes (bacteroides, Fusobacterium)
4. In neonates: Proteus and Citrobacter
5. Immunocompromised: fungi, protozoa (Toxoplasma, Nocardia, candida albcans, Listeria monocytogenes, Mycobacterium and aspergillus)

RISK FACTOR FOR CEREBRAL ABSCESS:

- Lung abnormalities (infection, AV fistula)
- Congenital coronary heart disease (R to L shunt)
- Bacterial endocarditis
- Penetrating head trauma
- Immunosuppression (AIDS)
- Dental abscess

CLINICAL FEATURES OF CEREBRAL ABSCESS:

Focal neurological signs and symptoms
- HA, Decreased LOC, hemiparesis, seizures in 50%
- Mass effect, increased ICP and sequelae (cranial enlargment in children)
- Systemic infection signs: low grade fever, leukocytosis

COMPLICATIONS OF BRAIN ABSCESS:

- With abscess rupture: ventriculitis, meningitis, venous sinus thrombosis
- CSF obstruction
- Transtentorial herniation

INVESTIGATIONS FOR BRAIN ABSCESS:

-CT scan often first test in ED
- MRI: imaging of choice (apparent diffusion coefficient differentiates abscess from tumour
- WBC/ESR may be normal, Blood cultures rarely helpful
- LP contraindicated if large mass
- CSF: non-specific, not usually helpful

TREATMENT OF BRAIN ABSCESS:

- Aspiration + excision and send for grain stain, AFB. C&S. fungal culture
- Excision perfeable if lovation suitable
- Abx: Vanco + Ceftriaxone + metronidazole or chloramphenicol or rifampin (6-8 wk)
- Revise ABx with C&S known
- Follow up CT is CRITICAL (weekly initailly)
- Mortality with appropriate therapy is 10%, permanent deficits in 50%

EXTRADURAL "EPIDURAL" HEMATOMA:

- Temporal-parietal skull fracture: 85% due to ruptured middle meningeal artery
- Remainder due to middle meningeal vein bleeding, dural sinus or bone/diploic veins
- Young adult male > female 4:1
- Rare before age of 2 and after 60

CLINICAL FEATURES OF EPIDURAL HEMATOMA:

- Classic (<30%)" post-traumatic reduced LOC, a lucid interval of several hours, then obtundation, hemiparesis, ipsilateral pupillary dilatation, and coma
- Signs and symptoms depend on severity but can include HA, NV, amnesia, altered LOC, HTN, Resp Distress
- Deterioration can take hours to days

INVESTIGATIONS FOR EPIDURAL HEMATOMA:

- CT without contrast: "lenticular shaped", usually limited to suture lines (Like a lens), bright white blood
- Compression of ventricles (midline shift)

TREATMENT OF EPIDURAL HEMATOMA:

- Admission, observation with serial CT if: small volume clot, minimal midline shift, (<5mm), GCS<8, no focal deficit
- Otherwise: Craniotomy to evacuate clot and follow up CT
- Mannitol pre-op if elevated ICP/brain herniation
- Good prognosis with prompt management (brain not damaged)
- WOrse if bilateral babinski or decerebration pre-op
- Death is usuallly due to respiratory arrest from uncal herniation and injury to midbrain

CEREBROVASCULAR DISEASE:

- 80% ISCHEMIC CEREBRAL INFARCTION: embolic, thrombosis of intracerebral arteries, vasculitis, hypercoagulability
- 20% INTRACRANIAL HEMORRHAGE: SAH, spontaneous ICH, IVH

SUBARACHNOID HEMORRHAGE:

- Bleeding into subarachnoid space
- Intracranial vessel between arachnoid and pia
- Traumatic (most common)
- Spontaneous:
1. Ruptured aneurysm 75-80%
2. Idiopathic 14-22%
3. AVM 4-5%
- Coagulopathy (iatrogenic or primary), vasculatides, tumours, cerebral artery dissections (<5%)
- 10-28/1000000 /yr
- Peak age 50-60, 20% of cases occur under age 45

RISK FACTORS FOR SAH:

- Hypertension
- Pregnancy/parturition in patients with pre-existing AVMs, eclampsia
- Oral contraceptive pill
- Substance abuse (cigarette, alcohol cocaine)
- Conditions associated with aneurysms

CLINICAL FEATURES OF SAH:

- SUDDEN onset of SEVERE "thunderclap" headache usually following exertion and described as the "worst headache of life"
- Nausea/vomiting, photophobia
- Meningismus (neck pain/stiffness, Kernig's Brudzinski's sign)
- Decreased LOC due to ischemia, ICP, seizure
- Focal deficit; cranial nerves III, IV, hemiparesis
- Ocular hemorrhage: 20-40% (due to sudden rise in ICP compressing central retinal vein
- Reactive hypertension

SENTINEL BLEEDS:

- Represents undiagnosed SAH
- SAH-like symptoms lasting < 1day
- May have blood on CT or LP
- 30-60% of full-blown SAH have a history suggestive of earlier sentinel bleed within past 3 weeks

DIFFERENTIAL DIAGNOSIS OF SAH:

- sentinel bleed
- Dissection/thrombosis of aneurysm
- Venous sinus thrombosis
- Benign cerebral vasculitis
- Benign exertional headache

FISHER GRADE OF SAH ON CT:

- GRADE 1: normal
- GRADE 2: < 1 mm thick
- GRADE 3: > 1 mm thick
- GRADE 4: SAH + ICH or IVH

HUNT AND HESS GRADE OF SAH:

- Clinical scale
- GRADE 1: No Sx or mild HA and or meningismus
- GRADE 2: Grade 1 plus CN palsy
- GRADE 3: Confusion/lethargy, mild hemiparesis or aphasia
- GRADE 4: GCS < 15 >8, moderate to severe hemiparesis, mild rigidity
- GRADE 5: Coma (GCS<9), decerebrate, morbibund appearance

INVESTIGATIONS FOR SAH:

1. NON-contrast CT
- May be negative if small bleed or presentation delayed for several days
- Acute hydrocephalus, IVH, ICH, infarct, or large aneurysm may be identified
2. LUMBAR PUNCTURE:
- Highly sensitive; for Dx when CT neg but high suspicion
- Bloody initially, xanthochromic supernatant with centrifugation ('yellow") by 12 hr, lasting 2 weeks
- RBC > 100000 without a difference between first to last tube
- Elevated protein due to blood breakdown
3. FOUR VESSEL ANGIOGRAPHY:
- gold standard for aneurysms
- Demonstrates source of SAH in 80-95% of cases
- Repeat angiogram in 7-14 d is negative first. Negative angio = perimesenchephalic SAH
4. MRA/CTA: 95% SEN for aneursysms

CT FEATURES OF SAH:

- Blood in BASAL CISTERNS
- Blood in SUPRACELLAR CISTERN
- Blood in Interhemispheric fissure
- Blood in Sylvian fissure
- Blood on surface of tentorium

TREATMENT OF SAH:

1. Admit to ICU
- oxygen/ventilation PRN
- NPO, bed rest, HOB @ 30, minimal external stimulation, neuro vitals q1h
- Maintain BP 120-150 (balance vasospasm prohylaxis, risk of rebleed, risk of hypotension since cerebral autoregulation impaired)
- Cardiac rhythm monitor, Foley PRN, MONITOR I/O
2. MEDICATIONS;
- IV NS with 20 KCl at 125-150cc/hr
- NIMODIPINE 60 mg PO/NG q4h x 21 d for vasospasm protection
- Seizure prophylaxis (Levetiracetam = Keppra) 500 mg PO/IV q12h x 1 wk
-Mild sedation PRN

COMPLICATIONS OF SAH:

1. VASOSPASM:
- vasoconstriction and permanent pathological vascular changes in response to vessel irritation from blood
- onset 4-14 day post SAH
- (delayed ischemic deficit) confusion, decreased LOC, focal deficit
- risk: large amounts of blood on CT, smoking, increases age, HTN
- Symptomatic vasospasm 20-30% SAH
- Radiographic vasospasm 30-70% SAH
- Diagnosed clinically and or transcranial doppler
- Risk of cerebral infarct/death
2. HYDROCEPHALUS
- 15-20%
- due to blood obstructing CSF drainage
- can be acute or choronic
- Requires drain or shunt
3. NEUROGENIC PULMONARY EDEMA
4. HYPONATREMIA:
- Due to cerebral salt wasting
5. DI
6. CARDIAC: arrhythmia, MI, CHF

TREATMENT OF VASOSPASM:

- Hyperdynamic TRIPLE H therapy using fluids, pressors after aneursym treated
-TRIPLE H: Hypertension, hypervolemia, hemodilution
- Direct vasodilation via angioplasty or intraarterial verapamil if refractory

PROGNOSIS OF SAH:

- 10-15% mortality before reaching hospital
- Overall 50% mortality, most within 2-3 wk
- 30% of survivors have moderate to severe disability
- Major cause of mortality is rebleeding
- Risk on rebleed: 4% first day, 15-20% in 2 weeks, 50% by 6 months
- After 6 months rebleed risk same as unruptured aneurysm (2%)
- Only prevention is early clipping of "cold" aneurysm
-

SUBDURAL HEMATOMA:

- SDH
- Acute vs chronic

ACUTE SDH:

- Caused by rupture of vessels that bridge the subarachnoid space (cortical artery, large vein, venous sinus) or cerebral laceration
- RISK: trauma, acceleration-deceleration injury, anti-coagulation,alcohol, cerebral atrophy, infant head trauma

CLINICAL FEATURES OF ACUTE SDH:

- No lucid period
- Signs and symptoms include altered LOC, pupillary irregularity, hemiparesis

INVESTIGATIONS FOR SDH:

- CT: hyperdence concave ("Crescnet") mass crossing suture lines

TREATMENT FOR ACUTE SDH:

- Craniotomy if clinically symptomatic, hematoma > 1cm thick, or midline shift > 5 mm
- Best to operate less than 4 hr
- otherwise observe with serial imaging

PROGNOSIS OF ACUTE SDH:

- Poor overall since brain parenchyma is often injured
- Mortality 50-90%, largely due to underlying brain injury
- Prognostic factors: initial GCS, neurological status, post-op ICP

CHRONIC SUBDURAL HEMATOMA:

- Many start out as acute SDH
- Blood within subdural space evokes inflammatory response
- Fibroblast invasion of clot and formation of neomembranes within days
- Growth of neocapillaries
- Fibrinolysis and liquefaction of clot
- Course is determined by balance of rebleeding from neomembranes and resorption of fluid

RISK FACTORS FOR CHRONIC SDH:

- Older
- Alcoholics
- Patients with CSF shunt, anti-coagulation, coagulopathy

CLINICAL FEATURES OF CHRONIC SDH:

-Often due to minor injury or no history of injury
- May present with minor HA, confusion, language difficulty, TIA-like symptoms
- Symptoms of raised ICP +/- seizures, progressive dementia, gait problems
- Obtundation disproportionate to neurological deficit: "great imitator" of dementia and tumour

INVESTIGATIONS OF CHRONIC SDH:

- CT: hypodense "liquefied clot" crescentic mass

TREATMENT OF CHRONIC SDH:

- Seizure prophylaxis only if post-traumatic seizure
- Reverse coagulopathy
- Burr hole drainage of liquefied clot if symptomatic or thickness > 1cm
- Craniotomy if recurs more than 2X
- Good overall prognosis as brain usually undamaged

INTRACEREBRAL HEMORRHAGE:

- ICH
- Hemorrahge within brain parenchyma, accounts for 10% of strokes
- Can dissect into ventricular system (IVH) or through cortical surfce (SAH)

ETIOLOGY OF ICH:

- HTN (usually causes bleeds at putaen, thalamus, pons, and cerebellum)
- hemorrhagic transformation (reperfusion post-stoke, surgery, strenuous exercise)
- Vascular abnormalities: Aneurysm, AVM
- Venous sinus thrombosis
- Arteriopathies (amyloid angiopathy, lipohyalinosis, vasculitis)
- Tumours (malignant: GBM, lymphoma, mets)
- Drugs (amphetamines, cocaine, alcohol, anticoagulants)
- Coagulopathy (iatrogenic, leukemia, TTP, anaplastic anemia)
- CNS infections
- Post trauma
- Eclampsia
- Post operative
- idiopathic

RISK FACTORS OF ICH:

- Increasing age (mainly > 55)
- Male gender
- HTN
- Black/Asian > caucasian
- Previous CVA of any type (23X risk)
- Both acute and chronic heavy alcohol use; cocaine, amphetamines
- liver disease
- Anticoagulants

CLINICAL FEATURES OF ICH:

- TIA like symptoms often precede ICH, can localize to site of impending hemorrhage
- Location: basal ganglia/internal capsule (50%), thalamus (15%), central white matter (15%), cerebellum/brainstem (usually pons) (15%)
- Gradual onset of symptoms over minutes to hours, usually during activity
- HA, NV, Decreased LOC common
- Specific symptoms and deficits depend on location of ICH

INVESTIGATIONS FOR ICH:

- Hyperdense blood on non-contrast CT
- CTA routine, if spot sign demonstrated there is high likelihood of cloth growth

MEDICAL TREATMENT OF ICH:

1. MEDICAL:
- decrease MAP to pre-morbid level or by ~20% (target 140/90)
- Check PTT/INR and correct coagulopathy
- Control raised ICP
- Levetiracetam/phenytoin for seizure prophylaxis
- Follow electrolytes (SIADH)
- Angiogram to R/O vascular lesions unless > 45 yrs, known HTN and putamen/thalamic/posterior fossa ICH

SURGICAL TREATMENT OF ICH:

- Craniotomy with evacuation of clot, treatment of source of ICH (AVM, tumour, cavernoma)
- Ventriculostomy to treat hydrocephalus
- 44% mortality in 30 days, most due to cerebral herniation
- Rebleed 2-6% higher if HTN poorly controlled

INDICATIONS FOR SURGICAL TREATMENT OF ICH:

- Symptoms of raised ICP or mass effect
- Rapid deterioration (especially if signs of brainstem compression
- Favourable location ( cerebellar, non-dominant)
- Young patient (<50yr)
- If tumour, AVM, aneurysm, or cavernoma suspected)

CONTRAINDICATIONS FOR SURGICAL TREATMENT OF ICH:

- Small bleed: minimal symptoms, GCS > 10
- Poor prognosis: massive hemorrhage (esp. dominant lobe), low GCS/coma, lost brainstem function
- Medical reasons (very elderly, severe coagulopathy, difficult location; basal ganglia, thalamus)

INTRACRANIAL ANEURYSMS:

- Prevalence 1-4% (20% have multiple)
- Female > male; age 35-65yr
- Saccular locations
1. ACOM 30%
2. PCOM 25%
3. MCA 20%
4. Basilar tip 7%

RISK FACTORS OF INTRACRANIAL ANEURYSMS:

- AD polycystic kidney disease (15%)
- Fibromuscular dysplasia (7-21%)
- AVMs
- Connective tissue disease (Ehlers-Danlos, Marfan's)
- Family history
- Bacterial endocarditis
- Osler-Weber-Rendu syndrome (hereditary hemorrhagic telangiectasia)
- Atherosclerosis and HTN
- Trauma

TYPES OF ANEURYSMS:

1. SACCULAR (berry)
- Most common
- Located at branch points of major cerebral arteries
- 85-95% in carotid system; 5-15% vertebrobasilar system
2. FUSIFORM:
- Atherosclerotic
- more common in vertebrobasilar system, rarely rupture
3. INFECTIOUS:
- Secondary to any infection of the vessel wall, 20% multiple
- 60% Strep and Staph
- 3-15% of patients with bacterial endocarditis

CLINICAL PRESENTATION OF INTRACRANIAL ANEURYSMS:

- Rupture (90%), most often SAG, but 30% ICH, 20% IVH, 3% subdural bleed
-SENTINEL HEMORRHAGE = "thunderclap headache" and requires urgent CLIPPING/COILING to prevent catastrophic bleed
- MASS EFFECT (giant aneurysms); may compress pituitary stalk/hypothalamus, optic nerve/chiasm causing visual defect, midbrain, pons, CNs
- Distal embolization (amaurosis fugax)
- Seizures
- Headache (w/o hemorrhage)
- Incidental CT or angiography finding

INVESTIGATIONS FOR INTRACRANIAL ANEURYSMS:

- CTA, MRA, Cerebral angiogram

TREATMENT OF RUPTURED ANEURYSMS:

- Early surgery or coiling (48-96 hr after SAH)
- Treatment options: surgical placement of clip, trapping, Coiling, wrapping
- Consider location, size, shape and tortuosity of aneurysms, patient comorbidities and presence of vasospasm for surgery vs coiling
- CLIPPING: superficial > deep, broad base, branching arteries and base, tortuosity, atheroscleorsis of afferent vessels, dissection, hematoma, acute brainstem compression
- COILING: posterior > anterior, deep, eloquent location, basilar artery bifurcation/apex, older age, presence of comorbidities, presence of vasospasm

TREATMENT OF UNRUPTURED ANEURYSMS:

- 1% annual risk of rupture; dependent on size and location on aneurysm
- No clear evidence on when to operate: need to weigh life expectancy
- Risk of morbidity/mortality of SAH (20-50% vs surgical risk (2-5%)
- Generally treat unruptured in > 10 mm
- Consider when 7-9 mm in middle aged, younger patients, or patients with family history
- Follow smaller aneurysms with serial angiography

VASCULAR MALFORMATIONS:

1. AVM
2. Cavernous malformations (cavernoama, cavernous hemangioma/angioma)
3. Venous angioma
4. Capillary teleangiectasia
5. AVF
6. Angiographically occult vascular malformations" (any type, 10% of malformations)

AVM:

- Tangle of abnormal vessels/arteriovenous shunts, with no intervening capillary bed or brain parenchyma, usually congenital
- Female 2:1, average age 33 yr
- 15-20% of patients with hereditary hemorrhagic telengiectasia will have cerebral AVM
- Spetzler Martin AVM grading scale: size, location, deep venous drainage

CLINICAL FEATURES OF AVM:

- Hemorrhage (40-60%): small AVMs are more likely to bleed due to direct high pressure AV connections
- Seizures (50%): more common with larger AVM
- Mass effect
- Focal neurological signs secondary to ischemia
- localized headache, increased ICP
- Bruit
- May be asymptomatic

INVESTIGATIONS FOR AVM:

- MRI (flow void), MRA
- Angiography (7% will also have one or more associated aneurysms)

TREATMENT OF AVM:

- Decrease risk of future hemorrahge and siezure
- Surgical excision is treatment of choice
- SRS is preferred for small (<3cm) or very deep lesions
- Endovascular embolization (glue, balloon) can faciltate surgery or SRS for larger lesions
- 10% mortality, 30-50% morbidity
- Risk of major bleed if untreated 2-4%

CAVERNOUS MALFORMATIONS:

- Benign vascular hamartoma consisting of irregular sinusoidal vascular channels located within the brain without intervening neural tissue or associated large vessels
- CCM1, CCM2 CCM3 genes
- 0.1-0.2% prevelance

CLINICAL FEATURES OF CAVERNOUS MALFORMATIONS:

- Seizures (60%), progressive neurological deficit (50%), hemorrhage (20%), HA
- Often an incidental finding
- Hemorrhage risk less than AVM, usually minor bleeds

MANAGEMENT OF CAVERNOUS MALFORMATIONS:

- T2WI MRI gradient echo sequencing best for diagnosis
- Surgical excision
- Only for symptomatic lesions that are accessible (supratentorial less likely to bleed)

ROOT COMPRESSION:

- herniated disc
- Neoplasm (neurofibroma, schwannoma)
- Synovial cyst, abscess
- Hypertrophic bone/spur

CERVICAL DISC SYNDROME:

- Nucleus pulposus herniates through annulus fibrosis and impinges upon nerve root, most commonly C6-C7

CLINICAL FEATURES OF CERVICAL DISC SYNDROME:

- Pain down arm in nerve root distribution, worse with extension, ipsilateral rotation and lateral flexion
- LMN signs and symptoms
- central cervical disc protrusion causes myelopathy as well as nerve root deficits

INVESTIGATIONS FOR CERVICAL DISC SYNDROME:

- If red flags, C spine, CT, MRI
- Consider EMG, nerve conduction symptoms if uncertain diagnosis

TREATMENT OF CERVICAL DISC SYNDROME:

1. CONSERVATIVE:
- No bedrest unless severe radicular symptoms
- Activity modification, patient education (reduce sitting/lifting)
- Physiotherapy, exercise program
- Analgesics, collar, traction may help
2. SURGICAL:
- Intractable pain despite adequate conservative treatment > 3 months
- Progressive neurological deficit
- Anterior cervical discectomy
= 95% improve spontaneously 4-8 wks

C4-5 DISC SYNDROME:

- Root C5
- 2 %
- Sensory: shoulder
- Motor: deltoid, biceps, supraspinatus
- Reflex: no change

C5-6 DISC SYNDROME:

- C6 root
- 19%
- Thumb sensation
- Biceps motor
- Biceps and brachioradialis reflexes

C6-7 DISC SYNDROME:

- C7 root
- 69%
- Middle finger sensation
- Triceps motor
- Triceps reflex

C7-T1 DISC SYNDROME:

- C8 root
- 10%
- Ring and 5th finger sensation
- Digital flexors motor
- Finger jerk (Hoffmann's sign)

RED FLAGS FOR BACK PAIN:

- BACKPAIN
- B: Bowel/bladder (retention or incontinence)
- A: Anesthesia of the saddle region
- C: Constitutional symptoms
-K: Khronic diease
- P: Parasthesia
- Age: > 50, < 20
- IV DU
- Neuromotor deficits

CAUDA EQUINA:

- Urinary retention or incontinence
- Fecal incontinence or loss of anal sphincter tone
- Saddle anesthesia
- Leg weakness/pain

MALIGNANCY OF SPINAL CORD:

- Age > 50
- Previous Hx of cancer
- pain unrelieved by bed rest
- constitutional symptoms
- Infection
- Increased ESR
- IVDU
- Immunosuppresion
- fever

COMPRESSION FRACTURE OF SPINE:

- Age > 50
- Trauma
- Prolonged steroid use

CERVICAL STENOSIS:

- Cervical spondylosis is chronic disc degeneration and associated facet arthropy
- Results in mechanical back pain, radiculopathy, myelopathy and combinations
- Typically begins at age 40-50, men > women, C5,6 > C6,7
- the spinal cord is pinched with neck extension
- With neck flexion, canal dimensions increase to relieve pressure on the cord

CLINICAL FEATURES OF CERVICAL STENOSIS:

- Insidious onset of mechanical back pain exacerated by excess vertebral motion
- Occipital headache is common
- Radiculopathy may invovle 1 r more roots
- Symptoms include neck. shoulder, arm pain parathesia, numbness
- WEAKNESS upper > lower extremity, decreased dexterity and sensory changes
- UMN: hyperreflexia, clonus, babinski's reflex
- Most worrisome complaint is lower extremity weakness (corticospinal tracts)
- Myelopathy may be associated with funicular pain, characterized by burning +/- stinging +/- LHERMITTE'S SIGN (lightning sensation down back with neck flexion)

INVESTIGATIONS FOR CERVICAL STENOSIS:

- X ray C spine +/- flexion, extension, oblique views: facet changes, osteophytes, disc space narrowing
- CT
- MRI
- EMG

TREATMENT OF CERVICAL STENOSIS:

- NSAIDS
- Moist heat
- Strengthening and ROM exercises
- Analgesics
- Cervical collar
- Traction
- SURGICAL: myelopathy with motor impairment, progressive neurological impairment and or intractable pain

LUMBAR DISC SYNDROME:

- Laterally herniated lumbar disc compresses nerve root
- Centrally herniated disc causes cauda equina or lumbar stenosis (neurogenic claudication)

CLINICAL FEATURES OF LUMBAR DISC SYNDROME

- leg pain > back pain
- Limited back movement due to pain, especially forward flexion
- Motor weakness, dermatomal sensory changes, reflex changes
- exacerbated by coughing, sneezing, straining.
- Relief with flexing of knew or thigh
- Nerve root tension signs:
1. SLR + Lasegue's or crossed SLR (L5,
S1)
2. Femoral stretch test (L2,3,4)

INVESTIGATIONS FOR LUMBAR DISC SYNDROME:

- X ray spine (r/o other lesions), CT MRI
- myelogram and post-myelogram CT only is MRI is contacindicated

TREATMENT OF LUMBAR DISC SYNDROME:

1. CONSERVATIVE same as cervical
2. SURGICAL indications
- Same as cervical disc + cauda equina
- 95% improve spontaneously in 4-8 weeks

L3,4 DISC SYNDROME;

- L4 root
-<10%
- Femoral pattern pain
- Sensory to medial leg
- Tib Ant motor (DF)
- Reflex Knee jerk

L4,5 DISC SYNDROME:

- L5 root
- 45%
- Sciatic pattern pain
- Dorsal foot to hallux and lateral leg sensory changes
- Extensor hullucis longus weakness
- Medial hamstring reflex loss

L5,S1 DISC SYNDROME:

- S1 root
- 45%
- Sciatic pain pattern
- Lateral foot sensory changes
- Gastrocnemius, soleus (plantar flexion) weakness
- Ankle jerk hyporeflexia

CAUDA EQUINA SYNDROME:

- Compression or irritation of lumbrosacral nerve roots below conus medullaris (below L2)
- Decreased space in the vertebral canal below L2
- Commonly caused by herniated disc +/- spinal stenosis, vertebral fracture and tumour

CLINICAL FEATURES OF CAUDA EQUINA SYNDROME:

- Usually acute (develops in less than 24 hr
- Motor (LMN) signs: weakness/paraparesis in multiple root distribution
- Reduced DTR to knee or ankle
- AUTONOMIC: urinary retention (or overflow incontinence) and/or fecal incontinence due to loss of anal sphincter tone
- SENSORY: Low back pain radiating to legs (sciatica) aggravated by Valsalva maneurver and by sitting...relieved by lying down
- Bilateral sensory loss of pain
- Saddle (S2-S5) anesthesia
- Sexual dysfunction (late)

TREATMENT OF CAUDA EQUINA SYNDROME:

- Urgent investigation and decompression (< 48 hr) to preserve bowel, bladder and sexual function and or to prevent progression to paraplegia
- Prognosis improves with surgical decompression
- Recovery correlates with function and initial presentation
- if patient is amubulatory, likely to stay ambulatory

LUMBAR SPINAL STENOSIS:

- Caused by congenital narrowing of spinal canal combined with degenerative changes (herniated disc, hypertrophied facet joints and ligamentum flavum)
- Gradually progressive back and leg pain with standing and walking that is relieved by sitting or lying down (neurogenic caludication= 60% SEN)
- Investigations: Cspine XR, CT, MRI, Myelogram if MRI contraindicated
- Tx: Conservative: NSAIDs, analgesia OR surgical: laminectomy with root recompresion

NEUROGENIC CLAUDICATION:

- Ischemia of lumbosacral nerve roots secondary to vascular compromise and increased demand from exertion; often associated with lumbar stenosis

CLINICAL FEATURES OF NEUROGENIC CLAUDICATION:

- Dermatomal pain/paresthesia/weakness of buttock, hip, thigh or leg initiated by standing or walking
- Slow relief with postural changes (sitting > 30 min), NOT simply exertion cessation
- Induced by variable degrees of exercise or standing
- May be elicited with lumbar extension, but may not have any other neurological findings, no signs of vascular compromise (Ulcer, poor cap refill)
- BICYCLE TEST distinguish neurogenic claudication from vascular claudication
- TREATMENT: same as for lumbar spinal stenosis

NEUROGENIC VS VASCULAR CLAUDICATION:

- NEUROGENIC CLAUDICATION: Dermatomal distribution with positional relief occurring over minutes
- VASCULAR CLAUDICATION:
Sclerotomal distribution with relief occurring with rest over seconds

SYRINGOMYELIA:

- "Syrinx"
- Cystic cavitation of spinal cord
- Presentation is highly variable, usually progresses over months to years
- Initially pain, weakness; later atrophy and loss of pain and temperature sensation

CAUSES OF SYRINGOMYELIA:

- 70% are associated with Chiari I malforamtion
- Post-traumatic
- Tumour
- Tethered cord

CLINICAL FEATURES OF SYRINGOMYELIA:

- Nonspecific for any intramedullary pahtology
1. Sensory loss similar to central cord syndrome (dissociated sensory loss)
2. Pain and temperature loss with preserved touch and joint sense in a band like distribution at level of syrinx
3. Dysesthetic pain often in distribution of sensory loss
4. LMN arm/hand weakness or wasting
5. Painless neuropathic arthropaties

INVESTIGATIONS FOR SYRINGOMYELIA:

- MR is best, myelogram with delayed Ct next
- Treat underlying cause (posterior fossa decompression for Chiarai I, surgical removal of tumour if causing syrinx)

COMPLETE SCI:

- Bilateral loss of motor/sensory and autonomic function at > 4 segments below below lesion/injury with UMN signs
- About 3% of pt with complete injuries will develop some recovery within 24 h

INCOMPLETE SCI:

- Any residual function > 4 segments below lesion
- Signs include SENSORY/MOTOR function in lower limbs and SACRAL SPARING
- SACRAL SPARING= perianal sensation, voluntary rectal sphincter contraction

TYPES OF INCOMPLETE SCI:

1. Brown- Sequard
2. Anterior Cord
3. Central cord (most common)
4. Posterior cord

BREOWN-SEQUAD SYNDROME:

- Hemisection
- Ipsilateral LMN weakness at lesion
- Ipsilateral UMN weakness below lesion
- Ipsilateral loss of vibration and proprioception
- Contralateral loss of pain and temperature
- Preserved light touch

ANTERIOR CORD SYNDROME:

- Anterior spinal artery compression of occlusion
- Bilateral LMN weakness at lesion
- Bilateral UMN weakness below lesion
- Urinary retention
- Preserved vibration and proprioception
- Bilateral loss of pain and temperature
- Preserved light touch

CENTRAL CORD SYNDROME:

- Syringomyelia, tumour, spinal hyperexension injury
- Bilateral motor weakness: Upper limb weakness (LMN) > than lower limb weakness (UMN)
- Urinary retention
- variable bilateral suspended sensory loss
- Loss of pain and temperature greater than loss of vibration and proprioception

POSTERIOR CORD SYNDROME:

- Posterior spinal artery infarction or trauma
- MOTOR PRESERVED
- SENSORY: Bilateral loss of vibration, proprioception, light touch at and below lesion
- Preserved pain and temp

CLASSIFICATION OF PERIPHERAL NERVE INJURY:

- SEDDON'S CLASSIFICATION
- CLASS I = NEURAPRAXIA
- CLASS II = AXONOTMESIS
- CLASS III = NEUROTMESIS

NEURAPRAXIA:

- Axon structurally intact but fails to function
- Recovery within hours to months (6-8 wk average)

AXONOTMESIS:

- axon and myelin sheath disrupted but endoneurium and supporting structures intact
- Wallerian degeneration of axon segment distal to injury
- Spontaneous axonal recovery at 1mm/d, max 1-2 years

NEUROTMESIS:

- Nerve completely transected, need surgical repair for possibility of recovery

CAUSES OF PERIPHERAL NERVE DAMAGE:

- Ischemia
- Nerve entrapment: compression my nearby anatomic structures, often secondary to localized, repetitive mechanical trauma with additional vascular injury to nerve

INVESTIGATIONS FOR PERIPHERAL NEUROPATHY:

- NEURO EXAM: power, sensation, reflexes), localization (TINEL'S)
- ELECTROPHYSIOLOGY: EMG, nerve conduction study (2-3 wk post injury)
- LABS: Blood work, CSF
- IMAGING: Cspine, Chest/Bone XR, myelogram, CT, MRI
- Angiogram if vascular damage suspected

TREATMENT OF PERIPHERAL NERVE ENTRAPMENT:

- Conservative: prevent repeated stress/injury, physio, NSAID, local anesthesia/steroid injection
- SURGICAL: nerve decompression +/- transposition for progressive deficits, muscle weakness/atrophy, failure of medical management

TREATMENT FOR PERIPHERAL NERVE STRETCH/CONTUSION:

- Follow up clinically for recovery
- Exploration if no recovery in 3 months

TREATMENT OF AXONOTMESIS:

- If not recovering, resect damaged segment
- Prompt physical therapy and rehab to increased muscle function, maintain joint ROM and maximize return of useful function
- Recovery usually incomplete

TREATMENT OF NEUROTMESIS:

- Surgical repair or nerve sheath unless known to be intact
- (suture directly or nerve graft with sural nerve)
- Clean laceration: early exploration and repair
- Contamination or associated injuries: tag initially with nonabsorbable suture, reapparoach within 10 d

COMPLICATIONS OF PERIPHERAL NERVE INJURY AND REPAIR:

- Neuropathic pain: with neuroma formation
- Complex regional pain syndrome: with sympathetic nervous system invovlement

INDICATIONS FOR INTUBATION IN TRAUMA:

1. Depressed LOC < 8
2. Need for hyperventilation
3. Severe maxillofacial trauma: patency of airway doubtful
4. Need for pharmacologic paralysis for evaluation or management
T = intubated on GCS

INITIAL MANAGEMENT OF TRAUMA PT:

- RAPID PRIMARY SURVEY:
1. Airway maintenance and cervical spine control
2. Breathing and ventilation
3. Circulation (pulses and hemorrhage control)
4. Disability (Neuro status)
5. Exposure (complete) and Environment (Temperature)
- Continually reassessed during secondary survey

AIRWAY MANAGEMENT WITH C SPINE:

- First secure
- Immobilize C spine
- Assess ability to breathe and speak
- Head tilt, jaw thrust
- ETT intubation
- Cricothyroidotomy

SIGNS OF AIRWAY OBSTRUCTION:

- Agitation, confusion, "universal choking sign"
- Respiratory distress
- Failure to speak, dysphoria
- Cyanosis

ASSESSING BREATHING:

1. LOOK: metnal status (anxiety, agitation, decreased LOC), colour, chest movement (bilateral vs. asymmetrical), respiratory rate/effort, nasal flaring
2. LISTEN: Sounds of obstruction (stridor), breathe sounds, symmetry or air entry, air escaping
3. FEEL: Flow of air, tracheal shift, chest wall for crepitus, flail segments, sucking chest wounds, subq emphysema
- Measure rate, O2, ABG, A-a gradient
- MANAGEMENT:
1. O2
2. Bag-Valve mask

ASSESSMENT OF CIRCULATION:

- Pulses and bleeds
- Control external bleeding (pressure, elevation)
- Consult surgery for internal bleeding
- Infuse 1-2L NS/RL through 2 large bore 14g IVs wide open
- Replace lost volume 3:1 with crystalloid
- Transfusion (severe hypotension, crystalloid not working, rapid bleed)

NEUROLOGICAL ASSESSMENT IN TRAUMA:

1. MINI HISTORY: Period of LOC, post-traumatic amnesia, loss of sensation/function, type of injury/accident
2. NEUROLOGICAL EXAM: GCS, H&N, Spine, Eyes, Brainstem, CN, Motor, sensory, reflexes, sphincter tone, record and repeat neurological exam at regular intervals

INVESTIGATIONS FOR NEUROLOGICAL TRAUMA:

- Spine precautions
- C,T,L, XR
- CT head and upper C spine
- Cross type, ABG, CBC, Drug screen
- Chest and pelvic Xray as indicated

TREATMENT OF MINOR HEAD INJURY:

- Observation over 24-48 h
- Wake every hour
- Judicious use of sedatives or pain killers during monitoring period

TREATMENT OF SEVERE HEAD INJURY (GCS<8):

- Clear airway and ensure breathing (GCS<8= intubate)
- Secure C spine
- Maintain adequate BP
- Monitor for clinical deterioration
- Monitor and manage increased ICP if present

WHEN DOES HEAD INJURY REQUIRE ADMISSION:

- Skull fracture
- Confusion, impaired consciousness, concussion > 5 min amensia
- Focal neurological signs, extreme headache, vomiting, seizures
- Unstable spine
- Use of alcohol
- Poor social support

ASSESSMENT OF SPINE CT/XR:

- ABCDS
- ALIGNMENT: anterior vertebral line, posterior vertebral line, spinolaminar line, posterior spinous line)
- BONE: Vertebral bodies, facets, spinous processes
- CARTILAGE
- DISC: space and interspinous space
- SOFT TISSUES

PATHOGENESIS OF HEAD INJURY:

- Acceleration/deceleration: contusions, subdural hematoma, axonal and vessel shearing, mesencephalic hematoma
- IMPACT: skull fracture, concussion, epidural hematoma
- PENETRATING: worse with high velocity and or high missile mass. Low velocity does damage to structures on entry. High velocity does damage away form missile tract.

SCALP INJRUY:

- Rich blood supply
- Considerable blood loss (vessels contract poorly)
- Minimal risk of infection due to rich vascularity

SKULL FRACTURES:

- Depressed fractures
- Simple fractures: "closed" no need for Abx, no surgery
- Compound fractures: "open" requires surgical debridement within 24hr
- Internal fractures into sinus may lead to meningitis or pneumocephalus
- Risk of operative bleed may limit treatment to Abx
- BASAL SKULL FRACTURES: Retroauricular ecchymoses, periorbital ecchymoses, hemotympanum, CSF rhinorrhea, otorrhea

CRANIAL NERVE INJURIES:

- Most traumatic causes of cranial nerve injury do not warrant surgical intervention
- Surgical intervention: CN II, III, IV, VIII (local eye/orbit, herniation, or repair of ossicles)
- Injuries that heal: I (months or none), III,IV, VI (most recover), VII (recovery with delayed lesions), VIII (vestibular over weeks, deafness permanent)

ARTERIAL BLEEDING IN HEAD TRAUMA:

- Carotid-Cavernous fistula, carotid/vertebral dissection
- Intracranial bleeding

PRIMARY IMPACT BRAIN INJURY:

- Mechanism of injury determines pathology: penetrating injuries, direct impact
- CONCUSSION: No abnromalities on CT . AAN grade 1 < 15 min grade 2 > 15 min, Grade 3 any loss of consciousness
- COUP (damage at site of blow) CONTRECOUP (damage at opposite side of blow): acute decompression causes cavitation followed by a wave of acute compression
- CONTUSION: high density on CT +/- mass effect. Commonly occurs when brain impacts bony prominence
- DIFFUSE AXONAL INJURY: tears in blood vessels (hemorrhagic foci) often the cause of decreased LOC if no space occupying lesion on CT

SECONDARY BRAIN INJURIES:

- Delayed and progressive injury to brain due to :
1. high glutamate release > NMDA > Cytotoxic cascade
2. Cerebral edema
3. Intracranial hemorrhages
4. Ischemia/infarction
5. Raised ICP/intracranial HTN
6. Hydrocephalus

EXTRACRANIAL CONDITIONS IN HEAD TRAUMA:

1. HYPOXEMIA: due to chest trauma, upper airway or brainstem. Leads to ischemia and raised ICP
2. HYPERCARBIA: leads to raised ICP
3. SYSTEMIC HYPOTENSION: loss of cerebral autoregulation leads to decreased CPP, ischemia
4. FLUID AND ELECTROLYTE IMBALANCE: - iatrogenic (most common)
- SIADH (head injury > hyponatremia)
- DI (hypernatremia)
- May lead to cerebral edema and raised ICP
5. COAGULOPATHY

BRAIN INJURY OUTCOMES:

- Mildly traumatic (GCS 13-15): post concussive symptoms (HA, fatigue, dizziness, nausea, blurred vision, diplopia, memory impairment, tinnitus, irritability, low concentration (50% at 6w wk, 14% at 1 yr)
- Moderate (GCS 9-12): proportional to age (> 40) and CT; 60% good recovery, 26% moderately disabled, 7% severely disabled, 7% vegetative/dead
- SEVERE (GCS < 8): difficult to predict, correlates with post-resuscitation GCS (esp motor) and age

LATE COMPLICATIONS OF HEAD/BRAIN INJURY:

- SEIZURES: 5% of head injury patients develop seizures
- Incidence related to severity and location
- Early seizures increases incidence of later seizures
- MENINGITIS: CSF leak from nose or ear
- HYDROCEPHALUS: acute hydrocephalus or delayed NPH

NEUROGENIC SHOCK:

- Hypotension that follows SCI
- BP less than 80
- Caused by interruption of symp below level of injury
- Loss of muscle tone due to Skm paralysis below level of injury (venous pooling)
- Blood loss from associated wounds

SPINAL SHOCK:

- Transient loss of a neurologic function below the level of the spinal cord injury
- Causes flaccid paralysis and areflexia for variable periods

WHIPLASH DISORDERS:

- Traumatic injury to soft tissue structures in the region of the cervical spine due to hyperflexion, hyperextension or rotational injury to the neck

SUSPECTING SCI:

- Major causes of death in SCI are ASPIRATION AND SHOCK
- Suspect SCI until proven otherwise: all significant trauma, or minor trauma + decreased LOC, neck or back pain, weakness, abdominal breathing, numbness/tingling or priapism

STABILIZATION AND MANAGEMENT OF SCI:

1. ABC, immobilization, oxygenation, foley catheter to urometer. DVT prophylaxis
2. Hypotension: maintain BP > 90 with pressor (dopamine), hydration, and atropine.
3. Monitor CBC and lytes
4. Focused history
5. Spine palpation: point tenderness or deformity
6. Motor level assessment: (including rectal exam)
7. Sensory level assessment
8. Evaluation of reflexes
9. Signs of autonomic dysfunction: perspiration, bowel, bladder, priapism
10. Radiographic: C spine, oblique, flexion extension, CT +/- MRI

MEDICAL MANAGEMENT SPECIFIC TO SCI:

- Methylprednisolone (given within 8 hr)
- +/- decompression in acute, non-penetrating SCI

FRACTURES/DISLOCATION OF THORACIC AND LUMBAR SPINE:

- Assess ligamentous instability using flexion/extension xray views of Cspine +/- MRI
- Thoracolubar spine unstable if 4/6 segments disrupted
- Anterior column: anterior longitudinal ligament
- Posterior column: supraspinous, interspinous and ligamentum ligaments

TYPES OF SPINAL FRACTURES:

- Denis classificaiton
1. Compression fracture (58%)
2. Burst fracture (17%)
3. Flexion distraction injury (6%)
4. Fracture-dislocation (6%)

COMPRESSION FRACTURE:

- Produced by flexion
- Posterior ligament complex and intervertebral joint capsules remain intact
- Fractures are stable, but lead to kyphotic deformity

BURST FRACTURE:

STABLE: anterior and middle columns parted with bone retropulsed nearby
- Hallmark is pedicle widening on AP XR
- Spinal cord; posterior column uninjured
2. UNSTABLE: same as the stable but with posterior column disruption

FLEXION DISTRACTION INJURY:

- Hyperflexion and distraction of posterior elements
- Middle and posterior columns fail in distraction
- Classic: CHANCE = horizontal fracture through posterior arch, pedicles, posterior vertebral body
- Can be purely ligamentous

FRACTURE DISLOCATION:

- Anterior and cranial dislocation of superior vertebral body = 3 column failure
1. Flexion-rotation
2. Flexion-distraction
3. Shear/hyperextension

C-SPINE FRACTURES:

1. C1 = JEFFERSION FRACTURE:
- Vertical compression of occipital condyles onto C1 pushing lateral masses outward and disrupting the ring of the atlas
2. C3 = ODONTOID PROCESS FRACTURE:
- Causes C1 and C2 to move independent of C2 body
- alar and transverse ligaments on posterior aspect of odontoid usually remain intact
- Present reporting a feeling of instability and holding their head with hands
3. C2 = HANGMAN FRACUTE:
- Traumatic spondylolisthesis of axis
- Bilateral fracture through the pars fo C2
- usually neurologically intact
4. CLAY-SHOVELER FRCTURE:
- Avulsion of spinous process of usually C6-C7

CLASSIFICATION OF ODONTOID FRACTURES:

- TYPE I: Through tip
- TYPE II: THrough base
- TYPE III: Through middle of vertebral body

IMAGING FOR CERVICAL FRACTURES:

- AP spine Xray
- Open mouth view
- Lateral view
- CT

TREATMENT OF CERVICAL FRACTURES:

- IMMOBILIZATION in cervical collar or halo vest until healing (2-3 months)
- Type II and III odontoid consider fixation of comminution, displacement, instability

NEUROLOGICALLY DETERMINED DEATH:

- Irreversible and diffuse brain injury resulting in absence of clinical brain function
- Cardiovascular activity may persists for up to two weeks

CRITERIA FOR NEUROLOGICALLY DETERMINED DEATH:

- Prerequisites: no CNS depressant drugs/neuromuscular block, no drug intoxication/poisoning, temperature > 32, no electrolyte/acid-base/endocrine disturbance
> Absent brainstem reflexes:
1. Absent pupillary light reflex
2. Absent corneal reflexes
3. Absent oculocephalic response
4. Absent caloric responses
5. Absent pharyngeal and tracheal reflexes
6. Absent cough with tracheal suctioning
7. Absent respiratory drive at CO2 > 60 or >20 above baseline (apnea test)
- 2 evaluations separated by time, usually by 2 specialists (anesthetist, neurologist, neurosurgeon)
- Confirming test: flat EEG, absent perfusion assessedwith cerebral angiogram

ALTERED LEVEL OF CONSCIOUSNESS HISTORY:

- Previous/recent head injury (hematoma)
- Sudden collapse (ICH,SAH)
- Cardiovascular surgery, prolonged cardiac arrest (hypoxia)
- Limb twitching, incontinence, tongue biting (seizure, post-itcal)
- Recent infection (meningitis)
- Other medical problems: DM, renal failure, hepatic encephalopathy
- Psychiatric illness (drug overdose)
- Telephone witnesses, read ambulance report, check medic-alter bracelet
- Neurologic symptoms: headache, visual changes, focal weakness)

PHYSICAL EXAMINATION FOR ALTERED LEVEL OF CONSCIOUSNESS:

- GCS
- PUPILS: reactive, symmetry, papilledema (ICP)
- REFLEXES: corneal, gag, oculocephalic, VOR, DTRs, Plantar reflex
- TONE
- SPONTANEOUS INVOLUNTARY MOVEMENTS
- ASSESS FOR MENINGEAL IRRITATION, INCREASED TEMP
- Assess for head injury, battle's sign, racoon eyes

COMA:

- An unarousable state in which patients show no meaningful response to environmental stimuli
- Lesions affecting cerebral cortex bilaterally, RAS or connection fibers
- Focal supratentorial lesions do not alter consciousness except by herniation or precipitating seizure

CLASSFICATION OF COMA:

- STRUCTURAL: (tumour, pus, blood, infection, CSF) 33% of comas. Supratentorial via herniation of infratentorial via direct compression or damage to RAS
- METABOLIC or DIFFUSE HEMISPHERIC DAMAGE:
1. Deficiency of essential (oxygen, glucose, VitB12)
2. Exogenous toxins (drugs, heavy metal, solvents)
3. Endogenous toxins (uremia, hepatic encephalopathy, electrolyte disturbance, thyroid storm)
4. Infections (meningitis, encephalitis)
5. Trauma (concussion, diffuse shear axonal damage)

INVESTIGATIONS AND MANAGEMENT OF COMA:

- ABC
- LABS: lytes, TSH, LFT, Cr, BUN, toxic screen, glucose
- CT, MR, LP, EEG

PERSISTENT VEGETATIVE STATE:

- a condition of complete unawareness of the self and the environment accompanied by sleep wake cycles with either complete or partial preservation of hypothalamic and brainstem autonomic function
- Awake but not aware
- Follows comatose state
- Most commonly caused by cardiac arrest or head injury
- Due to irreversible loss of cerebral cortical function but intact brainstem function
- Average life expectancy is 2-5 years

SPINAL DYSRAPHISM:

1. Spina bifida occulta
2. Meningocele (Spina Bifida Aperta)
3. Myelomeningocele (Spina Bifida Aperta)

SPINA BIFIDA OCCULTA:

- Congenital absence of a spinous process and a variable amount of lamina
- No visible exposure of meninges or neural tube
- 15-20% of the general population; most common L5, S1
- Caused by failure of fusion of the posterior neural arch
- No obvious clinical signs
- Presence of lumbosacral cutaneous abnormalities (dimple, sinus, port-wine stain, hair tuft)
- INVESTIGATIONS: plain film, US, MR to exclude spinal abnormalities
- NO TREATMENT

MENINGOCELE:

- Herniation of meningeal tissue and CSF through a defect in the spine, without associated herniation of neural tissue
- Primary failure of neural tube closure
- Most common in lumbosacral area
- Usually no disablity, low incidence of associated anomalies and hydrocephalus
- Plain films, CT, MR, US, ECHO, GU investigations
- Surgical excision and tissue repair

MYELOMENINGOCELE:

- Herniation of meningeal and CNS tissue through a defect in the spine
- Primary failure of neural tube closure
- Sensory and motor changes distal to anatomic level
- Urinary and fecal incontinence
- 65-85% of patients with Myelomeningocele have hydrocephalus
- Most have type II chiari malformation
- Plain films, CT, MRI, US, ECHO, GU investigations
- Surgical closure to preserve neurologic status and prevent CNS infections
- Closure in-utero shown to decrease hydrocephalus and improve post-natal motor scores
- 95% 2 year survival
- 80% have IQ > 80.
- 3-10% have normal urinary continence
- Early mortality due to chiari malformation complications (respiratory arrest and aspiration

PEDIATRIC HYDROCEPHALUS CAUSES:

1. CONGENITAL:
- Aqueductal anomalies, primary aqueductal stenosis in infancy
- Secondary gliosis due to intrauterine viral infections (mumps, varicella, TORCH)
- Dandy-Walker malformation (2-4%)
- Chiari malformation, especially type II
- Myelomeningocele
2. ACQUIRED:
- Post meningitis
- Post hemorrhage (SAH, IVH)
- Masses (vascular malformation, neoplastic)

CLINICAL FEATURES OF PEDIATRIC HYDROCEPHALUS:

- Symptoms and signs are are related
- Increased head circumference, bulging anterior fontanelle, widened cranial sutures
- Irritabiity, lethargy, poor feeding, vomiting
- "cracked pot" sound on cranial percussion
- Scalp vein dilation
- Sunset sign: forced downward deviation of eyes
- episodic bradycardia and apnea

INVESTIGATIONS FOR PEDIATRIC HYDROCEPHALUS:

- Skull XR, US, CT, MR, ICP monitoring

TREATMENT OF PEDIATRIC HYDROCEPHALUS:

- Same as adults

DANDY-WALKER MALFORMATIONS:

- Atresia of foramina Magendie and Luschka resulting in complete of incomplete agenesis of the cerebellar vermis with widely separated, hypoplastic cerebellar hemispheres
- Posterior fossa cyst, enlarged posterior fossa
- Dilation of 4th and other ventricles
- Associated with: Hydrocephalus (90%), agenesis of corpus callosum (17%), Occipital encephalocele (7%)
- accounts for 2-4% of pediatric hydrocephalus

CLINICAL FEATURES OF DANDY-WALKER MALFORMATION:

- 20% are asymptomatic
- Seizure in 15%
- Symptoms and signs of hydrocephalus combined with prominent occiput in infancy
- Ataxia, spasticity, poor fine motor control common in childhood

INVESTIGATION FOR DANDY-WALKER MALFORMATION:

- US
- CT
- MR

TREATMENT FOR DANDY-WALKER MALFORMATION:

- Asymptomatic require no treatment
- Associated hydrocephalus requires surgical treatment
1. VP shunt 2. CP shunt 3. LP shunt
4. VA shunt with lumbar drain
- 75-100% survival, 50% have normal IQ

CHIARI MALFORMATIONS:

- Malformations at the medullary-spinal junction
- Unclear cause, likely maldevelopment/degenesis during fetal life
1. TYPE I = Cerebellar ectopia
- Cerebellar tonsils lie below level of foramen magnum
- Average age of presentation is 15 years
2. TYPE 2
- Part of cerebellar vermis, medulla, and 4th ventricle extend through foramen magnum to midcervical region
- Presents in infancy

TYPE I CHIARI MALFORMATION:

- Tonsils below foramen magnum
- Presents later (15 yr)
- many asymptomatic
- Scoliosis
- Brain compression
- Central cord syndrome (65%)
- Syringomyelia (50%)
- Foramen magnum compression syndrome (20%)
- Cerebellar syndrome (1%)
- Hydrocephalus (10%)
- MRI
- Surgical decompression for symptomatic patients using suboccipital craniectomy, duraplasty

TYPE II CHIARI MALFORMATION:

- Vermis, medulla and 4th ventricle below foramen magnum
- Presents early (infancy)
- Always myelomingocele
- Findings due to brainstem and lower cranial nerve dysfunction
- Syringomyelia, hydrocephalus in >80%
- MRI
- Surgical decompression if neurogenic dysphagia, stridor, apneic spells using cervical laminectomy and duraplasty

CRANIOSYNOSTOSIS:

- Premature closure of cranial sutures
1. SAGITTAL: most common, long narrow head with ridging satgittal suture
2. CORONAL: expansion in superior and lateral direction (brachiocephaly)
3. METOPIC: (trigonocephaly)
4. LAMBDOID: least common
- 0.6/1000 live births, usually sporadic
- Familial incidence is 2% of sagittal and 8% of coronal synostosis

CLINICAL FEATURES OF CRANIOSYNOSTOSIS:

- Skull deformity
- Raised ICP +/- hydrocephalus
- Ophthalmologic problems due to ICP or bony abnormalities of the orbit
- Must differentiate between positional plagiocephaly (back sleeping)

INVESTIGATIONS FOR CRANIOSYNOSTOSIS:

- XR, CT

TREATMENT OF CRANIOSYNOSTOSIS:

- parental counselling about nature of deformity, associated neurological symptoms
- Surgery for cosmesis except in elevated ICP

PEDIATRIC BRAIN TUMOURS:

- 20% of all pediatric cancers
- 60% are infratentorial
1. GLIAL: astrocytoma (low-grade, anaplstic, glioblastoma multiforme)
2. PRIMITIVE NERVE CELLS: (Primitive neuroectodermal tumour (PNET)) 90% of neonatal brain tumours, medulloblastoma (infra), pineal gland
3. NON-NEURONAL CELL: germ cell tumour, craniopharyngioma, dermoid, meningioma, schwannoma, pituitary adenoma

RELATIVE FREQ OF PEDIATRIC BRAIN TUMOURS:

- Low grade astrocytoma (40%)
- Medulloblastoma (20%)
- Brainstem glioma (8%)
- Ependymoma (8%)
- Malignant glioma (6%)
- Craniopharyngioma (6%)
- PNET (4%)
- Pineal, germ cell (3%)

CLINICAL FEATURE OF PEDIATRIC BRAIN TUMOURS:

- vomiting, seizure, macrocrania, hydrocephalus
- Developmental delay, poor feeding, FTT
- Often initially escapes diagnosis due to expansile cranium and neural plasticity in children

MOVEMENT DISORDERS TREATED SURGICALLY:

1. Parkinson's disease
2. Dystonia
3. Tremor

SURGICAL TARGET OF PARKINSON'S DISEASE:

- For intractable contralateral bradykinesia/tremor, failure of medical management, drug-induced dyskinesias
- Simultaneous, bilateral surgery/stimulation is most common
- Anterodorsal Subthalamic Nucleus (STN)
- Can also stereotactically ablate (pallidotomy)/stimulation of GPi
- For parkinsonian tremor: stereotactic ablation and stimulation of ventral intermediate nucleus of thalamus (Vim)
- Morbidity: ICH, infection seizure 1-4%, psychiatric, paresthesias

SURGICAL TARGET FOR DYSTONIA:

- For contralateral primary dystonias; cervical and tardive dystonias (GPi)
- Contralateral secodnary dyskinesias: drug induced (L-dopa, neuroleptics STN)
- GPi ablation and stimulation for primary dystonia
- STN for secondary dystonia
- Risk: ICH, Infection, seizure (1-4%), cognitive functioning

SURGICAL TARGETS OF TREMOR:

- Contralateral appendicular essential tremor
- Intention tremor from demyelination of cerebellar outflow tracts (MS)
- Brainstem tumor
- Thalamotomy/stimulation of Vim nucleus of thalamus

NEUROPSYCHIATRIC DISORDERS WITH SURGICAL TREATMENTS:

1. Obsessive compulsive disorders
2. Tourette's
3. Major Depressive Disorders

SURGICAL TARGETS FOR OCD:

- For severe symptoms refractory to medical management
- Anterior capsulotomy and stimulation of anterior limb of internal capsul
- 25-75% response rate
- ICH (1-2%), mild effects on cognitive funciton, anxiety +/- panic disorder

SURGICAL TARGETS FOR TOURETTE'S:

- For severe symptoms refractory to medical management
- Stimulation of midline intralaminar nuclei of the thalamus
- Stimulation of motor and limbic portions of GPi
- stimulation of anterior limb of IC
- >70% reduction in vocal or motor tics +urge
- ICH (1-2%), mild sexual dysfunction

SURGICAL TARGETS OF MDD:

- Severe depression refractory to medical management and ECT
- Stimulation of subgenual cingulate cortex
-60% response. 35% remission
- ICH (1-2%), pain, headache, worsening of mood and irritability

CHRONIC PAIN TREATED WITH SURGERY:

1. Neuropathic
2. Nociceptive

SURGICAL TARGETS FOR NEUROPATHIC PAIN:

- Severe, intractable, organic neuropathic pain (post-stroke, phantom limb, trigeminal neuralgia,
- Stimulation of contrallater VPL, VPM thalamic nuclei +/- PVG PAG
- 47% improvement in perception of pain intensity
- Less favourable for central pain syndromes or poorly localized pain symptoms
- ICH 1-2%, paresthesia, anxiety, panic disorder

SURGICAL TARGETS FOR NOCICEPTIVE PAIN:

- For severe, intractable organic nociceptive pain
- Bilateral stimulation of PAG, PVG
- 63% improvement in pain intensity
- ICH (1-2%), paresthesia, anxiety, panic

INDICATIONS FOR SURGICAL MANAGEMENT OF EPILEPSY:

- Medically refractory seizures (2 first line drugs)
- identification of distinct epileptogenic region through history, EEG, MRI and neuropsychological testing
- If not localized, may be candidate for palliative corpus callosotomy

SURGICAL PROCEDURES TO TREAT EPILEPSY:

- Adults: resection of hippocampus and parahippocampal gyrus
- Children: resection of epileptogenic space occupying lesion
- Hemispherectomy and corpus callosotomy are less common

OUTCOME OF SURGERY FOR EPILEPSY:

- 41-79% of adults seizure free for 5 years after temporal lobe resection
- 58-78% children seizure free after surgery
- Surgery is associated with improvements in preexisting psychiatric conditions

MORBIDITY FROM SURGERY FOR EPILEPSY:

- 0.4-4% partial hemianopsia, aphasia, motor deficit, sensory deficit or CN palsy
- Some decline in verbal memory for dominant or visuospatial memory for non-dominant
- Memory decline stabilizes after 1-2 yrs
-

SURGICAL TREATMENT FOR TRIGEMINAL NEURALGIA:

- For refractory to medical management
1. TRIGEMINCAL NERVE BRANCH local block (phenol, alcohol), neurectomy
2. NERVE BRANCHES v1 (supraorbital), v2 (foramen rotundum), v3 (foramen ovale)
3. PERCUTANEOUS TRIGEMINAL RHIZOTOMY with glycerol or mechanotrauma
4. Radiofrequency themocoagulation
5. Gamma knife
6. Microvascular decompression

ATIVAN:

- For status epilepticus
- 4 mg IV over 2 min and q10-15min
- Not exceeding 8mg/12h

CARBAMAZEPINE:

- For trigeminal neuralgia or seizures

PHENYTOIN:

- "dilantin"
- For seizures and status epilepticus

DEXAMETHASONE:

- For cerebral edema, head injury, pseudotumor cerebri
- Pre-op for ICP secondary to brain neoplasms (except lymphoma)

MANNITOL:

- 1-1.5g/kg IV rapid
- For raised ICP

NIMODIPIDE:

- For vasospasm in SAH

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