Undergraduate Neurosurgery Lecture Notes

[CONTENTS]
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Contents
CONTENTS 1
CLINICAL EXAMINATION 7
History taking 7
Symptoms 7
Examination 9
Conscious level assessment 9
Higher cerebral function examination 10
Cognitive skills 10
Memory test 11
Cranial Nerve examination 12
Gait 15
Reflexes: 17
Sphincters 17
Differential diagnosis between UMNL and LMNL 18
Sensory examination: 18
Coordination: 20
Special tests 21
CONGENITAL ANOMALIES 22
Types of Congenital Anomalies: 22

Cranial Anomalies 22
Spinal Anomalies 23
Hydrocephalus 25
CSF Circulation 25
Infantile hydrocephalus 26
Adult hydrocephalus 27
Normal pressure hydrocephalus 27
Craniosynostosis 29
Myelomenigocele 31
Meningocele 33
HEAD TRAUMA 34
Concussion 34
Scalp hematoma (cephalhematoma) 35
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2 [PRINCIPLES OF NEUROSURGERY]
Skull fractures 35
Vault fractures 35
Skull base fractures 37
Growing skull fractures 38
Brain edema 39
Diffuse axonal injury (DAI) 40
Intracranial hemorrhage 41
Extra dural hematoma 41
Brain shift 43
Subdural hematoma (SDH) 44
Subacute subdural hematoma 45
Subdural hematoma in infancy 46
Intracerebral hematoma 47
Management of head injuries 48
SPINAL CORD COMPRESSION 50
Pathology 50
Causes 50
Clinical presentation 51
Spinal cord syndromes 51
SPINAL FRACTURE 54
Epidemiology 54
Etiology 54
Mechanisms of: spinal injury 54
Pathology 55
Vertebral column injuries 55
Cord and root injuries 56
Clinical picture 57
Management 57
DEGENERATIVE SPINAL DISORDERS 59
Cervical disc prolapse 59

Anatomy 59
Pathophysiology 59
Clinical picture 60
Investigations 61
Management 62
[CONTENTS] 3
Cervical spondylosis 63
Clinical picture 63
Investigations 63
Management 63
Lumbar disc prolapse 64

Anatomy 64
Pathophysiology 64
Clinical picture 64
Cauda equina syndrome 66

Presentation 66
Investigations 66
Treatment 68
Lumbar canal stenosis 70

Types 70
Clinical picture 70
Management 70
Lumbar spondylolithesis 71
Treatment 71
BRAIN TUMORS 72
Overview 72
WHO Classification of CNS tumors 72

Tumors of neuroepithelial tissue 73
Tumors of the meninges 74
Germ cell tumors 74
Cysts and tumor like conditions 74
Pituitary tumors 75
Craniopharyngioma 75
Medulloblastoma 76
Clinical Picture of brain tumors 76

Frontal lobe tumor 76
Parietal lobe tumors 76
Temporal lobe tumors 77
Investigations 78
Radiological investigations 78
Laboratory investigations 79
Lines of treatment of brain tumors 79

Surgical excision 79
Biopsy 79
Conventional Radiotherapy 79
Stereotactic Radiosurgery 79
Proton Beam therapy 79
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Chemotherapy 80
Medical treatment 80
CEREBRAL ABSCESS 81
Epidemiology 81
Risk factors 81
Sources of infection 81
Presentation 82
Evaluation 82
Staging of cerebral abscess 83
Treatment 83
CEREBROVASCULAR DISORDERS 85
Stroke 85
Definition 85
Ischemic Stroke 86
Classification 86
Clinical Presentation of Ischemic Stroke 86
Imaging 87
Treatment 89
Management for acute ischemic stroke: 89
Hemorrhagic stroke 91
Etiology: 91
Clinical Picture 91
Investigations 92
Treatment 92
Aneurysms 93
Definition 93
Prevalence 93
Clinical Presentation 94
Subarachnoid Hemorrhage 94
Mass Effect 94
Cerebral Ischemia 94
Asymptomatic Unruptured Intracranial Aneurysms 94
Diagnostic Imaging 95
Treatment 97
Brain arteriovenous malformations (AVMs) 97

Definition 97
Natural History 97
Clinical Presentation 98
Intracranial Hemorrhage 98
Epilepsy 98
Headache 98
[CONTENTS] 5
Focal Neurologic Deficits 98

Diagnostic Imaging 98
Treatment 99
PERIPHERAL NERVE DISORDERS 100
Entrapment Neuropathy 100

Carpal Tunnel Syndrome 100
Differential diagnosis 101
Management: 101
Ulnar Entrapment at the Elbow (Cubital tunnel syndrome) 102
Management 102
Differential diagnosis 103
Meralgia Paresthetica 104
The condition can also be due to: 104
Management 104
Tarsal Tunnel Syndrome 105
Management 105
Thoracic outlet syndrome 106
Management: 106
Traumatic Lesions 107

Pathology (types) 107
Concussion (Neuropraxia) 107
Contusion (Axonotemesis) 107
Complete disruption (Neurotemesis) 107
Types of traumatic agent 107
Upper Limb Nerves Injuries 108

Brachial Plexus Injury 108
Upper plexus (trunk) paralysis (Erb–Duchenne type) 108
Lower plexus (trunk) paralysis (Dejerine–Klumpke type) 109
Injuries in the axilla 110
Musculocutanous nerve 110
Radial nerve 110
Median nerve 110
Ulnar nerve 110
Injuries of the arm and the forearm: 111
Radial nerve in the spiral groove (lateral injury) 111
Posterior interosseus injury in the forearm 111
Medial nerve injury (medial injury) 111
Ulnar nerve injury (medial injury) 112
Ulnar paradox 113
Wrist and hand injuries 113
Median nerve injury 113
Ulnar nerve injury 113
Lower Extremities Injuries 114

Femoral nerve injury 114
Sciatic nerve injury 114
The common peroneal nerve 114
The tibial nerve 114
The Sciatic nerve 114
Management of traumatic nerve injuries 115
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FUNCTIONAL NEUROSURGERY 116
Tools used in functional neurosurgery 116

Radiosurgery 118
The use of functional neurosurgery for the management of pain 119

Cranial procedures 119
Trigeminal neuralgia 119
Other sources of pain 119
Spinal procedures 119
Low back pain 119
Cancer pain 120
The use of functional neurosurgery for the management of involuntary movements: 121
Lesioning techniques: 121
Stimulation techniques using deep brain stimulation: 121
Radiosurgery: 121
The use of functional neurosurgery for the management of epilepsy: 122

Stimulation techniques: 122
Radiosurgery: 122
The use of functional neurosurgery for the management of psychological disorders

(psychosurgery): 122
The use of functional neurosurgery for the management of spasticity: 123

[CLINICAL EXAMINATION] 7
Clinical Examination
History taking
Important in establishing the diagnosis, and must be taken in conjunction with

information from other systems, previous medical history, family and social
history.
Symptoms
Headache:
- Onset and course (sudden/ gradual)
- Duration
- Frequency
- Severity in a scale from 1 to 10 (10 being the severest headache in the
patients life as headache due to rupture aneurysm).
- Timing: morning headaches are more common in brain tumors
- Site: is it migraine? Is it related to the nasal sinuses
- Character: throbbing, band like.
- Aggravating and alleviating factors
- Associated features: (vomiting, visual disturbances, excessive lacrimation)
Visual disorders:
- Onset, course, duration, frequency, aggravating and alleviating factors
- Impairment
o One/both eyes
o Partial/ total visual loss
o Whole/ partial field loss
- Hallucinations and illusions
Speech/language disorders
- Difficulty in articulation (dysartheria)
- Difficulty in expression (expressive dysphasia)
- Difficulty in understanding spoken words (receptive dysphasia)
- Difficulty in reading (dyslexia)
- Difficulty in writing (dysgraphia)
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Motor
- Lack of Coordination
- Weakness
o Progressive/static
o Proximal/ distal
o Painful/ painless
- Involuntary movements
Sensory Disorder
- Pain
- Numbness/tingling
- Hyperthersia
Sphincters:
- Incontinence (which type?)
- Retention
Lower Cranial nerves

- Deafness/ tinnitus
- Vertigo
- Balance/staggering
- Swallowing difficulty
- Change in voice
Mental disorder
- Memory
- Intelligence
- Personality
- Behavior
Examination
Conscious level assessment
The Glasgow coma scale is the best-known scoring system; it depends upon the
eye opening, verbal RESPONSE and motor RESPONSE. It is widely used
results are reproducible irrespective of the status of the observer and can be
carried out by paramedics as by clinicians.
Area assessed Response Score
Eye opening Spontaneous 4

To Speech 3
To pain 2
None 1
Best Verbal response Oriented 5
Confused conversation 4
Inappropriate words 3
Incomprehensible sounds 2
None 1
Best motor response Obey Commands 6
Localizes pain 5
Withdrawal (normal flexion) 4
Abnormal flexion (decorticate) 3
Extension (decerebrate) 2
None 1
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Higher cerebral function examination
Cognitive skills
Dominant hemisphere:
- Dyphasia (listen to the patient’s language pattern)

o Expressive: if the patient is hesitant, unable to compose phrases
(non fluent aphasia with intact comprehension) = impairment of the
Broca’s area (Broca’s is broken Boca)
o Receptive aphasia: fluent aphasia with impaired comprehension,

patient talks but his words do not make sense = impairment of the
Wernicke’s area (Wernickes is Wordy but make no sense)
o Conductive Aphasia: poor repetition, but the patient had fluent

speech and intact comprehension = impairment of the arcuate
fasiculus that connect Broca’s, Wernickes areas
o Global Aphasia: Nonfluent aphasia with impaired comprehension =

impairment of both Wernicke’s and Broca’s areas
o Nominal aphasia: patient is unable to name objects
- Dyslexia: patient can not read correctly
- Dysgraphia: patient can not write correctly
- Dyscalculia: patient will not be able to serially subtract 7 from 100
- Agnosia:
o Visual agnosia: patient is unable to identify seen objects
o Tactile agnosis: patient is unable to identify objects in his hands
with closed eyes
Non-dominant hemisphere
- Geographical agnosia: inability of the patient to find his way around the
ward
- Apraxia: in ability of the patient to perform complex movements
o Dressing apraxia
o Constructional apraxia: inability of the patient to copy a geometrical
pattern as the drawing of a cube.
Memory test
Cannot be done in confused or dysphasic patients
- Immediate memory: ask the patient to repeat the sequence of 5 to 7

random numbers
- Recent memory: ask the patient to present his illness and duration of
hospital stay
- Remote memory: ask the patients about events and circumstances more
than 5 years old
- Verbal memory: ask the patient to remember a sentence or a short story
- Visual memory: ask the patient to remember objects on a tray and test
after 15 mins
NB:
• Retro grade amnesia: loss of memory of events leading up to a brain
injury or an insult
• Post traumatic amnesia: Permanent loss of memory of events for a
period following a brain injury
Reasoning and problem solving
- Two step calculation

- Ask the patient to revere 3 to 4 random numbers
- Ask the patient to explain proverbs
Emotional state
- Anxiety or excitement
- Depression or apathy
- Uninhibited behaviors should be recorded
- Slowness of movement or responses
- Personality type
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Cranial Nerve examination
Olfactory (I)
Test both perception and identification using aromatic non-irritant material (to
avoid the stimulation of the trigeminal nerve) e.g coffee, tobacco
NB: each nostril should be tested separately
Optic (II)
- Visual acuity:
- Visual fields:
- Fundus examination
o Look for clarity of the edges of the optic disc for papilloedema
NB: Papilledema on one side and optic atrophy on the other side in
anterior cranial fossa space occupying lesion is called Foster-Kennedy
syndrome.
Occulomotor (III)
- Pupils:
o Size, shape
o Equality
o Reaction to light
o Reaction to accommodation
- Ptosis
- Occular movement
Trochlear (IV)
Ask the patient to look downward and medially to test the superior oblique
Abducens (VI)
Ask the patient to look laterally to test the lateral rectus.
Conjugate movement: Note the ability of the patient’s eyes to move together in
the horizontal and the vertical directions.
Nystagmus: Slow drift to one direction and followed by fast “corrective”

movement. Nystagmus direction is usually described in terms of the fast phase.
Trigeminal nerve (V)
Test the three divisions and compare both sides
Pain
Temperature
Light touch
Corneal reflex:
Afferent: Trigeminal nerve.

Efferent: Facial nerve.
Motor:
Ask the patient to clamp his jaws
Feel the temporalis and masseter muscles
Open the jaw against resistance,
Check the jaw jerk for bilateral UMNL
Facial nerve (VII)
Ask the patient to:

- Wrinkle the forehead (frontalis)
- Close his eyes while the examiner attempts to open it (orbicularis occuli)
- Purse his lips (buccinators)
- Show his teeth (orbicularis oris
- Taste: by using sugar or NaCl
Auditory nerve (VIII)
Cochlear component
- Whisper numbers in one ear while masking the other ear by rubbing the
external meatus.
- Differentiate between conductive and perceptive deafness by
o Weber’s test: hold the base of 512 Hz tuning fork against the vertex
and ask the patient if the sound is heard more loudly in one ear. (in
conductive deafness the sound will be louder in the affected ear).
o Rinne’s test: hold the base of a vibrating 512 Hz tuning fork against
the mastoid bone. When the note disappears hold the tuning fork
near the external meatus. Patient should hear sound again since
the air conduction via the ossicles is better than bone conduction.
§ In conductive deafness, bone conduction will be better than air
conduction.
§ In nerve deafness, both are impaired.
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Glossopharyngeal nerve (IX), Vagus nerve (X)
Both nerves are examined together and their actions are seldom individually
impaired.
- Note the patient’s voice:

- Note any swallowing difficulty or nasal regurgitation of fluids
- Ask the patient to open his mouth and say Ah to check asymmetry of
palatal movements or deviation of the uvula (uvula will be deviated to the
opposite direction).
- Gag reflex: touch the posterior 1/3 of the tongue, palate, pharynx or tonsil
using a tongue depressor and check if the patient develops gag reflex
Accessory nerve (XI)
- Sternomastoid: ask the patient to rotate head against resistance. Compare

the power and muscle bulk on each side (NB the left sternomastoid turns
the head to the right side and vice versa)
- Trapezius: ask the patient to shrug his shoulders. Compare the power and
bulk on both sides
Hypoglossal nerve (XII)

- Inspect the tongue for any deviation (NB the tongue will be deviated to the
same side of the lesion)
- Ask the patient to push your fingers through his cheeks by his tongue.
Gait
Different forms of gait occurs with different pathologies as in the table
Gait Disease
Parkinsonian Gait (short steps, the Parkinson's disease
patient cannot easily stop as if he is Major tranquilizers
running after his center of gravity,
decreased arm swinging)
Marche a petits pas Gait Bilateral diffuse cortical dysfunction
Scissoring Gait Spastic paraparesis as in:
• Cerebral palsy
• Multiple sclerosis
• Cord compression
Waddling Gait Proximal myopathies
Bilateral congenital hip dislocation
Hemiplegic Gait (Circumduction Gait) Stroke
Sensory ataxia (+ve Rombergism) Peripheral neuropathy

Posterior column affection
Cerebellar ataxia (-ve Rombergism) Cerebellar pathologies
Antalgic Gait Painful limb Gait
Motor examination: to examine the motor power of different groups of

muscles in the upper and lower limbs including shoulder flexors, extensors,
adductors and abductors, elbow flexors and extensors, wrist flexors and
extensors, radial, ulnar grip and small muscles of the hand, hip flexors,
extensors, abductors and adductors, knee flexors and extensors, dorsiflexors,
planter flexors, invertors and evertors of the ankle joint.
Diagnostic approach to motor weakness
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Quadriparesis Upper motor neuron Cervical cord lesion

(weakness of all 4 lesion (UMNL) Brain stem lesion
limbs) Bilateral cerebral lesions
Lower motor neuron Polyradiculopathy
lesion (LMNL) Peripheral neuropathy
Mixed UMNL & LMNL Motor neuron disease
Muscle myopathy
Hemiparesis UMNL (only) Hemisection of the
(unilateral upper and cervical cord(sensory
lower limb weakness) signs present)
Brain stem lesion(brain
stem sign)
Cerebral lesion
(hemisphere signs)
Paraparesis UMNL Spinal cord lesion above
(weakness of both L1 & below C7
legs) Mixed UMNL & LMNL Conus medullaris
syndrome at L1
LMNL Cauda equina syndrome
below L1
Monoparesis (single UMNL Cortical lesions
limb weakness)
Non-anatomical LMNL Mononeuropathy,
distribution of Radiculopathy
weakness Muscle Functional weakness
Myasthenia gravis
Motor power grading according to medical research

council scale (MRC)
5 = Normal power
4 = Moderate movement against resistance
3 = Moves against gravity but not resistance
2 = Moves with gravity eliminated
1 = Flickers
0 = No movement
Muscle tone:
Hypertonia (spasticity): as in UMNL.
Hypotonia (flaccidity) : as in LMNL & cerebellar lesions.
Rigidity : as in extrapyramidal syndromes common causes include parkinsonism.
Reflexes:
Reflexes can be divided into:
Deep tendon reflexes

Reflex Root Nerve
Upper limb Biceps C5 - (C6) Musculocutaneus
Supinator C6 – (C5) Radial
(brachioradialis
muscle)
triceps C7 Radial
finger C8 Median & ulnar
Lower limb knee L3 –L4 Femoral

ankle S1 –S2 Tibial
Face Jaw reflex Trigeminal nerve

N.B if any reflex is unobtainable directly, ask the patient to do a reinforcement
manoeuvre.
Superficial reflexes which includes
1. Abdominal reflexes (upper & lower)

2. Planter reflex (babinski sign)
3. Cremasteric reflexes
Sphincters
Urinary sphincteric disturbances as retension with overflow incontinence,
spasticbladder.
Fecal sphincteric disturbance either incontinence or constipation
Impotence
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Differential diagnosis between UMNL and LMNL
UMNL LMNL
Tone Hypertonia Hypotonia
Wasting Minimal Maximal
Fasciculation Absent Present
Clonus Present Absent
Reflexes Hypereflexia Hyporeflexia
Abdominal reflex Absent Present
Planter reflex +ve Babineski sign Flexors
Hoffman sign +ve -ve
Sphincters Spastic bladder Retention with overflow

incontinence
Sensory examination:
Types of sensations:
1. Superficial sensations:
a. Pain & temperature (lateral spinothalamic tracts)
b. Crude touch (anterior spinothalamic tract)
2. Deep sensations: joint position, joint movement, vibration sense and

pressure sense (AKA proprioceptive sensations)(Gracile and Cuneate
tracts of the posterior column).
3. Cortical sensation: tactile localization, tactile discrimination and

stereognosis.
Dermatomal supply of the body
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Diagnostic approach to sensory loss
Sensory loss The most probable diagnosis
In the distribution of a single nerve Mononeuropathy
In the distribution of a single root Radiculopathy
Affecting both lower limbs with NO Peripheral neuropathy

clear sensory level
Affecting both lower limbs with a Spinal cord lesion

clear sensory level
Affecting both upper and lower Peripheral neuropathy

limbs with Glove and stocking
hypothesia
Affecting both upper and lower Cervical spinal cord lesion

limbs with a clear sensory level
and NO Glove and stocking
hypothesia
Hemisensory loss including the Thalamic lesion

ipsilateral face Internal capsule lesion
Hemisensory loss including the Brain stem lesion

contralateral face
Coordination:
Tests for coordination include:
• Finger nose test (we monitor dysmetria and decomposition of movement)
• Finger to finger test
• Finger to doctor's finger test (to detect mild forms of incoordination)
• Heal-knee-shin test
• Trunk can be tested for incoordination by asking the patient to sit from
lying without using his hands and observing if he fall to one side.
Abnormal movements: should be noticed as the presence of tremors,

myoclonus, chorea, hemiballismus, tics and dystonia.
Special tests
Meningeal irritation signs:
• Neck rigidity
• Kernig's sign
• Brudzinski's sign (neck to leg and leg to leg test).
Tests for lumbosacral radicular entrapment as in lumbar

disc prolapsed:
• Straight leg raising up test (SLRT)

• augmented SLRT
• Crossed SLRT
• Femoral stretch test
Tests for assessment of peripheral nerve functions as in

peripheral nerve injuries
• Paper test (in ulnar nerve injury)

• Card board test (in ulnar nerve injury)
• Pencil test (in median nerve injury)
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Congenital anomalies
Learning Objectives:
1. Identify different types of congenital anomalies
2. Define individual anomalies
3. Recognize underlying causes
4. Describe different clinical presentations and diagnostic procedures
5. Determine different treatment modalities
Remember
Congenital lesions of the CNS include:
1. Congenital anomalies i.e. developmental disorders
2. Congenital vascular lesions ex. cerebral aneurysms, cavernous
malformation
3. Congenital tumors ex. neurofibromatosis, neuroblastoma
Types of Congenital Anomalies:
Cranial Anomalies:
1. Encephalocele: This is a cystic malformation in which CNS

structures in communication with CSF pathways herniated through a
cranial defect.
2. Craniosynostosis: It is the premature fusion of one or more cranial

sutures separating the membranous bones of the skull.
3. Arachnoid Cyst: This is a collection of CSF surrounded by a

membrane resembling the arachnoid mater.
4. Agenesis of Corpus Callosum: It is complete absence of the

corpus callosum with distortion of the ventricles
5. Arnold-Chiari Malformation: It is chronic herniation of the

hindbrain through the foramen magnum. Four types are recognized; Chiari
type I-IV
[CONGENITAL ANOMALIES] 23
6. Dandy-Walker Cyst: This is cystic dilatation of the fourth ventricle

with varying degrees of agenesis of the cerebellar vermis.
7. Aqueductal Stenosis: This entails narrowing of the aqueduct of

Sylvius with dilatation of the supratentorial ventricular system.
8. Congenital Hydrocephalus: It is the abnormal increase in CSF

volume within the brain ventricles resulting in ventricular dilatation that
usually presents after birth with an enlarged head.
Spinal Anomalies:
1. Spina bifida occulta: This is a posterior bony defect of the

vertebra due to incomplete closure of the laminar arch. The skin overlying
the defect is often marked with a colored nevus or tuft of hair.
2. Meningocele: This is herniation of a sac of dura and arachnoid filled
with CSF outside the confines of the spinal canal through a localized
posterior spina bifida.
3. Myelomeningocele: This is herniation of dysplastic neural tissue in
a dural lined sac filled with CSF through a localized posterior spina bifida.
4. Myeloschisis: This is complete dehiscence of the neural tube
manifesting as gross defect in neurulation involving neural, osseous and
cutaneous structures.
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5. Congenital Spinal Dermal Sinus: This is an epithelium-lined

tract in the midline along the spine that forms a potential communication
between the skin surface and the deeper tissues. It may be found
anywhere from the midsacrum to the cervical area and may terminate in
the subcutaneous tissues, on the posterior elements of the spine, in the
epidural or intradural space, or in the neural elements.
6. Lumbosacral Lipoma: This is a subcutaneous lipoma that overlies
the lumbar or sacral spine, and extends through a posterior spina bifida to
an extradural or intradural location to attach to a low-lying conus
medullaris, the cauda equina, or the filum terminale.
7. Sacrococcygeal Teratoma: A teratoma is a congenital tumor
that develops from totipotential cells in the area of Hensen's node, which
migrated caudally to lie within the coccyx.
8. Tethered Cord Syndrome: This consists of an abnormally low
conus medullaris tethered by one or more forms of intradural abnormality.
9. Diastematomyelia: This is partial or complete division of a variable
length of the spinal cord into two hemicords of more or less equal caliber.
In complete cases, a septum of bone, cartilage or fibrous tissue is present
between the hemicords in which case each hemicord is surrounded by its
own dural sheath. In partial forms, no septum is present and a single dural
tube usually surrounds both hemicords. When the split does not reunite
distally the condition is referred to as “diplomyelia”.
10. Congenital Syringomyelia: It is tubular dilatation of the central
canal within the spinal cord extending over many segments.
Hydrocephalus
Definition: It is a hydrodynamic disorder of CSF circulation characterized by

abnormal increase in CSF volume within the brain ventricles with or without
associated increase in intracranial pressure.
CSF Circulation:
CSF is produced by filtration from the choroid plexus in the lateral and fourth
ventricles. It passes from the lateral ventricles through the foramina of Monro to
the third ventricle. Then it passes through the aqueduct of Sylvius to the fourth
ventricle. The main volume of CSF then passes through the central foramen of
Magendi and lateral foramina of Luschka to the subarachnoid space where it is
absorbed though the arachnoid villi and granulations into the superior sagittal
sinus. A small volume of CSF exits the fourth ventricle to the central canal of the
spinal cord.
Causes:
1) Congenital causes
1. Genetic-induced hydrocephalus "Bicker's-Adams syndrome"
2. In utero infections
3. In utero ischemic events
4. Aqueductal stenosis
5. Arnold-Chiari malformation "Type II & III"
6. Dandy-Walker cyst
7. Arachnoid cyst
2) Acquired causes
1) Post-meningitic
2) Intracerebral hemorrhage
3) Subarachnoid & intraventricular hemorrhage
4) Brain tumors
Pathogenesis:
1) Obstruction
• Mass obstruction: This due to block of ventricles by tumor or hemorrhage
• Flow obstruction: This is due to increased CSF viscosity mainly due to
increased proteins as in post hemorrhagic and post infectious.
2) Malabsorption
• Agenesis or hypoplasia of arachnoid villi and granulations
• Superior sagittal sinus venous thrombosis or obstruction
3) Hypersecretion
Choroid plexus hyperplasia or papilloma
4) Exvacu
This is due to atrophy of the periventricular brain mantle
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Pathology “Classification”:
According to the underlying cause and mechanism of ventricular dilatation,
hydrocephalus is classified into 2 types;
1. Communicating “Non-obstructive”
- Agenesis or hypoplasia of arachnoid villi and granulations
- Choroid plexus hyperplasia or papilloma
- Post-meningitic
- Post-hemorrhagic
2. Non-communicating “Obstructive”
- Aqueductal stenosis
- Brain tumors
Clinical Picture:
Infantile hydrocephalus
This type occurs in infants before closure of the skull sutures.
It is manifested by:
1. Poor suckling & feeding and high pitched cry.
2. Abnormal progressive enlargement of the head i.e. abnormal increase in
the head circumference more than the normal percentile for age
characterized by being bilateral, symmetrical and globular with
cephalofacial disproportion.
3. Separation of skull sutures.
4. Wide, tense, bulging fontanelles, specially the anterior fontanelle.
5. Dilated scalp veins.
6. Loss of upward gaze “Parinaud’s sign”, which further proceeds to
downward deviation of the eyeballs "sun-set appearance"
7. Cranial nerve palsies specially the VI nerve.
8. Seizures.
9. Late in the course, there may be UMN paraparesis which is explained by
stretch & ischemia of the descending periventricular lower limb fibers or
due to associated syringomyelia.
10. Delayed developmental milestones.
2) Adult hydrocephalus
This type occurs in children and adults after closure of the skull sutures.
It is manifested by symptoms and signs of increased intracranial pressure:
1. Headache
2. Vomiting
3. Blurred vision
4. Bilateral papilledema
5. Impaired consciousness
MRI Brain: showing dilated (left side) vs non-dilated (right side) ventricles
3) Normal pressure hydrocephalus

This type occurs in elderly patients.
It is manifested by triad of; i- dementia, ii- gait disturbance & iii- urinary
incontinence
Diagnostic Studies:
Plain skull radiography: shows large skull with cephalofacial disproportion and
widely separated sutures and fontanelles
CT brain & MRI brain: show the dilated ventricles and the cause of obstruction
in non-communicating hydrocephalus.
Differential Diagnosis:
i) D.D. of enlarged head “Macrocrania”
1. Familial
2. Hydrocephalus
3. Bone disease ex. rickets
4. Arachnoid cyst
5. Infantile chronic subdural hematoma
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Treatment: Strictly Surgical
Aim:
1. Treatment of the cause

2. CSF diversion i.e. shunting
Procedures:
a) Elimination of the obstructing lesion

- Excision of brain tumor
- Evacuation of intracerebral hematoma
b) Placement of shunt device
· Ventriculoperitoneal
· Ventriculoatrial
· Ventriculopleural
· Lumboperitoneal shunt
c) Endoscopic procedures
- Endoscopic aqueductoplasty
· Endoscopic third ventriculostomy
Complications of Shunt devices:

1· Infection
• Ventriculitis
• Peritonitis
• Pseudocysts
• Endocarditis
2· Obstruction
3· Disconnection
• Migration
• Intestinal perforation
• Extrusion
4· Overdrainage
• Subdural hematoma
• Craniostenosis
·
Craniosynostosis
Definition:
It is the condition in which one or more of the fibrous sutures in an infant skull
prematurely fuses by ossification, thereby changing the growth pattern of the
skull. Because the skull cannot expand perpendicular to the fused suture, it
compensates by growing more in the direction parallel to the closed sutures.
Types:
1. Metopic Synostosis: There is ridging of the metopic suture with
bilateral flattening of the frontal bones and anterior displacement of the coronal
suture. The resultant deformity is termed "Trigonocephaly".
2. Sagittal Synostosis: There is ridging of the fused sagittal suture with
frontal & occipital bossing and flattening of parietal bones. The head is elongated
anteroposteriorly. The deformity is termed "Scaphocephaly".
3. Unicoronal Synostosis: There is ridging of half of the coronal suture
and flattening of the ipsilateral frontal and parietal bones. The orbit is deformed
due to elevation of the sphenoid ridge and is commonly described as the
"harlequin eye" The deformity is termed "Anterior Plagiocephaly"
4. Bicoronal Synostosis: There is ridging of the coronal suture and
flattening of the caudal portion of the frontal bones and supraorbital ridges. The
skull is broad and short, with expansion in the lateral directions and bilateral
harlequin configuration of the orbits. The deformity is termed "Brachycephaly". It
may be part of congenital craniofacial syndromes “Apert syndrome or Crouzon
syndrome”.
5. Lambdoid Synostosis: There is ridging of the fused lambdoid suture
with flattening of the parieto-occipital region ipsilateral to the fused suture. The
deformity is termed "Posterior Plagiocephaly".
6. Pansynostosis (Craniostenosis):
The skull assumes a towering shape. The deformity is termed "Oxycephaly".
29
Normal (a) verses sagittal suture synostosis (b)
Clinical Manifestations:
A) Cosmetic disfigurement
B) Neurological
This is more common when two or more sutures undergo premature fusion.
- Restrained brain growth. This may result in mental retardation, motor
impairment, and optic atrophy.
- Increased intracranial pressure. The estimated risk of increased ICP
with different synostoses was as follows; 50% in pansynostosis, 26%
in bicoronal synostosis, 12% with unicoronal synostosis, 8% with
sagittal and 6% with metopic.
Differential Diagnosis:
- Microcephaly
- Postnatal positional molding
Investigations:
Plain skull radiography: Shows the suture fusion and the associated cranial
and orbital deformity, if present.
CT/MRI brain: Required in patients with coronal, metopic, or lambdoid
synostosis. It may show associated intracranial anomalies such as
hydrocephalus, agenesis of the corpus callosum.
Treatment:
Operative management
1) Synostectomy i.e. reopening of the prematurely closed suture.
2) Cranial remodeling & orbital advancement in selected cases.
Myelomenigocele
This is a herniation of dysplastic neural tissue in a dural lined sac filled with CSF
through a localized posterior spina bifida. The most common site is the
lumbosacral region.
Clinical picture:
This is the most common form of spinal dysraphism. The protruding sac is
usually covered with a translucent membrane of modified meninges and skin
called the “placode”. The lesion is soft, but the fluid usually cannot be
compressed easily from the sac into the spinal canal owing to the small
communication with the subarachnoid space. Transillumination produces poor
glow. The head circumference may be enlarged due to associated
hydrocephalus. Neurological examination shows variable degrees of motor
weakness, sensory deficits and sphincteric disturbances.
Differential diagnosis:
- Meningocele
- Lipomyelomeningocele
- Lumbosacral lipoma
- Sacrococcygeal teratoma
31
Investigations:
1. Plain spine radiography

- Posterior spina bifida
- Widened interpedicular diameter of the spinal canal at the level of the
defect.
2. MRI Spine
- Deformity
- Associated syringomyelia
- Associated tethered cord
3. MRI Head & Craniocervical junction
- Hydrocephalus.
- Chiari malformation
Treatment:
- Prevention through dietary supplementation with folic acid.
- Excision of the sac, untethering of the cord and repair of the dysraphic
defects.
MRI lumbosacral: showing Meningoencephalocele with neural contents inside.

Meningocele
This is a herniation of a sac of dura and arachnoid filled with CSF through a
localized posterior spina bifida. The most common site is the lumbosacral region.
Clinical picture:
The protruding sac is usually covered with normal skin. The lesion is soft, and the
fluid is compressed easily from the sac into the spinal canal. Transillumination
produces a brilliant glow. The head circumference is usually normal, and the
anterior fontanelle is lax because active hydrocephalus is rare in the immediate
neonatal period. Neurological examination is usually normal.
Diagnosis & Treatment:

Similar to myelomeningocele.
Myelomeningocele Meningocele
Overlying skin Defective Intact

Consistency Doughy Soft
Compressibility Partially compressible Totally compressible
Transillumination Partially illuminated Totally illuminated
Neurological deficits Associated deficits Intact
Associated 65% -
hydrocephalus
MRI lumbosacral showing empty meningocele
33
Head Trauma
Epidemiology
It is considered to be a major cause of death. It occurs at all age groups and in

young adults. Males are more affected than females
Causes of head injuries
1- Road traffic accidents (most common)

2- Assault by blunt or sharp object
3- Falling from a height
4- Falling of a heavy object over the head
5- Blast injuries
6- Birth injuries
Injuries are classified into 2 main groups:
Simple head injury:
Means concussion without scalp, bone or brain injury.
Compound head injury:
Head injury associated with scalp wounds, bone fractures and/or brain
injury.
Concussion
It is derived from the Latin word “concutere” which means to shake.
It means transient loss of consciousness after head trauma without evidence of
brain damage.
- It is followed by complete recovery
- May be associated with retrograde amnesia for less than 24 hrs.
[HEAD TRAUMA] 35
Scalp wounds:
Types
- Cut wounds
- Contused, lacerated wounds
- Penetrating wounds
Scalp hematoma (cephalhematoma)

It means blood collection under the scalp, usually it resolves spontaneously
without aspiration or drainage. It may be:
- Subcutaneous
- Subperiosteal: (stop at the suture line)
- Subgalial: moves freely between the subtemporal line, supraorbital
ad superior nuchal line à the cause of black eye.
Skull fractures:
Vault fractures:
Types:
a. Fissure (linear) fracture.
b. Depressed simple or comminuted fracture
In the above types, the fracture may be

a. Simple: i.e. without and external wound
b. Compound: i.e with an external wound and risk for infection
35
Depressed comminuted fracture
Treatment
a. In fissure fractures without complications (i.e. underlying hematoma) no

surgical treatment is required, just close observation not to develop
underlying extradural hematoma.
b. Depressed and comminuted fractures: The fracture site is explored and
the depressed fracture must be elevated to its original site. Debridement
will be required in compound fractures.
Indications for elevation of depressed fracture include:
- Depression is > 1 cm
- Gross cosmetic deformity
- Wound infection or gross wound contamination
- Frontal sinus involvement
- Clinical or radiological evidence (CT) of dural penetration (CSF leak
intradural pneumocephalus … etc)
- Presence of significant intracranial hematoma.
[HEAD TRAUMA] 37
Skull base fractures
It may include cranial nerve injuries and more commonly injury of the basal dura
with cerebrospinal fluid fistula formation.
Classified into:
a. Anterior cranial fossa fracture:

C/P:
- Epistaxis, CSF rhinorrhea
- Subconjuntival hemorrhage, Raccon’s eyes (periorbital hematoma)
- Olfactory nerve affection
Racoon eyes
b. Middle cranial fossa fracture:

C/P
- Bleeding per ear
- CSF otorrhea
- Affection of 7th and 8th cranial nerves
c. Posterior cranial fossa fracture:

C/P
- Battle sign: bluish color behind the ear
- Brain stem affection
- Atlanto axial subluxation
Battle sign
Treatment of skull base fractures:
Broad-spectrum antibiotic must be given to safe guard against meningitis,

especially, in cases with CSF leak.
Cranial nerve repair may be done in some cases as the facial nerve.
37
Growing skull fractures
A fracture that is associated with posttraumatic meningocele or

meningoencephalocele that occur in children. The cyst lies in between the bone
edges and by continuous pulsations, the fracture gap grows and widens.
Treatment:
Repair of the post traumatic cyst, but, if the gap is wide, cranioplasty is indicated
either by an artificial material or bone graft.
Growing skull fracture
The pathological processes involved in head trauma are:
1. Direct trauma
2. Brain edema
3. Brain contusion
4. Intra cranial hemorrhage
5. Intra cerebral shearing (diffuse axonal injury)
6. Hydrocephalus
Direct trauma
Occurs in penetrating head injuries; in contrast with blunt trauma which produces
wide spread effect.
[HEAD TRAUMA] 39
Brain edema
Definition: Increase of the interstitial fluid in the brain leading to the increase
of intracranial pressure, which could be focal or diffuse
Causes:
- Disturbance of the vasomotor tone

- Hypoxia, hypercapnia
- Electrolyte imbalance
Treatment
Position: elevation of the head of the bed 30 – 45 degrees

Proper ventilation and endotracheal intubation
Dehydrating medications:
• Mannitiol infusion at 1 gm/kg
• Lasix (frusemide) at 40 mg/12hrs
ICP monitoring: using external ventricular drainage

High dose barbiturate
Surgical: Unilateral brain edema can be treated by decompressive craniectomy
and extension duroplasty.
Cerebral contusion: a bruise of the brain tissue, which can be

associated with multiple microhemorrhages, small blood vessel leaks into brain
tissue.
Cerebral Laceration is a similar injury except that the pia-

arachinoid membranes are torn over the site of injury in laceration and are not
torn in contusion.
Burst lobe is an extensive contusion associated with subdural

hematoma.
39
Coup and countercoup injuries comprise a group of

focal brain injuries. The coup injury occur under the impact point while the contr-
coup injuries occur at areas distant from the point of impact as a result of shock
waves across the brain causing stress/cavitations effects.
Diffuse axonal injury (DAI)

Despite the absence of any intracranial mass lesion or history of hypoxia, some
patients remain unconscious after a TBI. The usual cause for persistent
impairment of consciousness is the condition referred to as diffuse axonal injury.
Diffuse axonal injury (DAI) is the result of traumatic shearing forces that occur
when the head is rapidly accelerated or decelerated. It results in injury of the
axons at the interface between the grey and the white matter.
Hydrocephalus
Which can be:
Non-communicating: due to obstruction of the 4th ventricle by blood clot or

cerebellar swelling
Communicating: due to subarachnoid hemorrhage that will decrease the
absorption from the arachnoid villi.
[HEAD TRAUMA] 41
Intracranial hemorrhage
Classified into
1. Extradural hematoma (EDH)

2. Subdural hematoma (SDH)
3. Subarachnoid hemorrhage (SAH)
4. Intracerebral hemorrhage (ICH)
5. Intraventricular hemorrhage (IVH)
Extra dural hematoma

More common in the younger age group as the dura is able to strip more readily
from the overlying bone. Associated with fissure fractures in 90 % of the cases
Source of bleeding:
• Arterial: middle meningeal artery

• Venous:
o Middle meningeal vein
o Venous sinuses
o Diploic veins
Site: CT brain: Temporal EDH

• 75% in the temporal area (due to
middle meningeal vessels)
• 25% in the frontal, parietal, occipital and posterior fossa areas
Clinical presentation
It can be:
- Slowly accumulating
- Rapidly accumulating
a. Slowly accumulating EDH:

The patient will pass through the following stages
§ Stage of concussion
§ Stage of lucid interval: the interval in which the patient
regains his consciousness after concussion and before it is
lost once more in the stage of compression
§ Stage of compression
41
b. Rapidly accumulating: the patients present with stage of

compression
Stage of compression:
- Signs of increased intracranial pressure: severe headache,

vomiting and deterioration of the level of consciousness
- Signs of lateralization due to (Uncal herniation)
o Ipsilateral dilated fixed pupil

o Ipsilateral conjugate eye deviation
o Contralateral hemiparesis
o Contralateral exaggerated reflexes and positive Babiniski
[HEAD TRAUMA] 43
Brain shift
Occurs with any space occupying lesion
Types:
1. Subfalcine herniation (a): no clinical effect
2. Tentorial herniation:
a. Lateral tentorial herniation (uncal herniation) (b):
Fixed dilated ipsilateral pupil due to compression of the 3rd nerve.
b. Central tentrial herniation (c):
i. Deterioration of the level of consciousness
ii. Diabetes insipidus
iii. Bilateral initially constricted then dilated pupils.
c. Tonsillar herniation (e)
More depression of the level of consciousness and cushing triad:
• Hypertension
• Bradycardia
• Cheyne-stoke breathing
•
Diagnosis of EDH
CT scan is the best diagnostic tool: It will show hyperdense biconvex hematoma
with compression of the underlying brain, and may cause distortion of the lateral
ventricle
43
Treatment
Considered as a surgical emergency and will result in death if not removed

promptly.
Urgent evacuation of the EDH is required through craniotomy, stopping of the
source of bleeding using (bipolar coagulation, gelfoam, bone wax and dural hitch
stitches)
Subdural hematoma (SDH)
Three types: (acute, subacute and chronic)
Acute subdural hematoma (less than 3 days)
Usually presents in the context of a patient with severe head injury whose
neurological state is either failing to improve or deteriorating.. Over 80% have
associated fracture of the cranial vault or the skull base
Source of bleeding
Commonly arises from cortical laceration or focal tear of a cortical artery.
Diagnosis
CT brain: white (hyperdense) concave hematoma
CT brain: Acute subdural hematoma

[HEAD TRAUMA] 45
Treatment
Considerable sizes should be evacuated surgically by craniotomy, if associated

with severe edema and midline shift, decompressive craniectomy will be done
and extension duroplasty. NB: generally, it has a bad prognosis
Subacute subdural hematoma (4 – 21 days)
CT brain: isodense concave hematoma
Chronic subdural hematoma (more than 21 days)
Usually it occurs in old patients (atrophic mobile brain) on anticoagulant. Bilateral

in 25 % of the cases
Source of bleeding
Bridging veins
Old patients with gradual development of a neurological deficit ( contralateral

weakness or dysphasia) with history of trivial trauma. However, it may happen
without history of trauma.
Diagnosis
CT brain: Hypodense concave hematoma usually large in size with midline shift.
CT brain: Chronic subdural hematoma
45
Treatment
Old hematomas are liquefied, therefore evacuation is done through burr hole and
postoperative adequate hydration (IV fluids).
NB: generally it has a good prognosis
Subdural hematoma in infancy
Birth trauma. It occurs also in battered children, violent shaking of an infant may
be sufficient to lacerate bridging veins.
Site
Bilateral in 85% of the cases and usually over the frontoparietal area
Usually presents with large size head (as the sutures are non-fused) and non
specific symptoms as irritability and failure to thrive.
Diagnosis
CT scan: bilateral concave isodense/hypodense hematomas
CT Brain: bilateral subdural collection

Treatment
Can be done by aspiration, which can be repeated. Refractory subdural

collection (hygroma) can be treated by subduro-peritoneal shunt.
[HEAD TRAUMA] 47
Intracerebral hematoma
Occurs either as a result of penetrating injury (missile injury), a depressed

fracture or following a severe head injury.
Clinical presentation.
Depends upon the site and the size of hematoma
Diagnosis
CT scan will show the size and the position of the hematoma
CT brain: temporal intracerebral hematoma

Treatment
Depends upon the site and the size of the hematoma as well as its clinical
presentation
Indications for surgery
o Large sized superficial hematoma causing mass effect (brain shift

and increase intracranial pressure)
o Posterior fossa hematoma as it is a very tight space
47
Management of head injuries
- THE ABC: maintenance of adequate Airway, Breathing and

Circulation
- Accurate neurological assessment
- Evaluation of other injuries (spine, chest, fractures)
- Urgent transfer to hospital
Neurological assessment
1. Evaluation of the level of consciousness through the Glasgow Coma

Score (GCS).
2. Assessment of signs of lateralization (pupils and neurological deficit)
3. Determine the cause, site and type of traumatic brain injury
The Gasgow Coma Scale (See the table in the clinical examination chapter)
The 15 points GCS is the most commonly used neurologic injury severity scale
for adults because of its high inter-observer reliability and generally good
prognostic capabilities.
Severity of TBI: It’s generally agreed that TBI with a GCS of 13 or above is
considered to be mild, 9 – 12 is considered to be moderate and 8 or below is
considered to be severe TBI.
NB: Intubation is mandatory if the GCS <8 as the patient will not be able to
protect his airway.
Investigations
Laboratory:
- CBC
- Blood grouping for expected blood transfusion
- Coagulation and bleeding profiles
- ABG (arterial blood gases)
[HEAD TRAUMA] 49
Radiological
- Plain X-ray skull

- Plain X-ray cervical spine
- Plain X-ray chest and U/S abdomen if needed for associated
injuries in major trauma especially in road traffic accidents
- CT scan brain: Gold standard in diagnosis of traumatic brain Injury
- MRI brain: have some value in diagnosis of diffuse axonal injury
49
Spinal cord compression
It is a common neurosurgical problem. Compression of the cord can occur at any

level from the cervicomedulary junction to the conus medullaris at L1. If this
condition is unrecognized and untreated the eventual outcome will be disabling
paralysis and sphincteric disturbance.
Pathology
The spinal cord can be compressed by:
a. Extradural lesions in 80%

b. Intradural, extramedullary lesions in 15%
c. Intradural, Intramedullary lesions in 5%
Causes
A. Traumatic:
a. Fracture spine
b. Hematoma
c. Traumatic disc
B. Tumors
a. Extradural: e.g metastasis and lymphoma
b. Intradural extramedullary: e.g. meningioma and neurofibroma
c. Intradural intramedullary: e.g. ependymoma and astrocytoma
C. Infection
a. Acute: e.g. staphylococcal
b. Chronic: TB which can be extradural or intradural
D. Disc Diseases and spondylosis (see the chapter of degenetrative spine
disorders
E. Hematoma: All can be extradural, intradural or intramedullary
a. AVM
b. Spontaneous
F. Congenital Cystic lesions
a. Intradural extra medullary: arachnoid cyst
b. Intradural intra medullary: syringmyelia
[SPINAL CORD COMPRESSION] 51
1. Pain
a. Root: severe, sharp, shooting, burning pain radiating into the
cutaneous distribution or muscle group supplied by the root;
aggravated by movement, straining or coughing.
b. Segmental: continuous, deep aching pain radiating into whole leg or
one half of the body; not affected by movement.
c. Bone: continuous dull aching pain and tenderness over affected area;
may or may not be aggravated by movement.
2. Neurological deficit:
a. According to the level of compression

i. Cervical spine à spastic quadriparesis with manifestations of
UMNL in upperlimbs and lower limbs
ii. Doral spine à s[astic paraparesis or paraplegia with manifetations

of UMNL in the lower limbs
iii. Conus medullaris à paraparesis or paraplegia with mixture of

UMNL and LMNL manifestations in the lower limbs
b. According to the part of the cord compressed:
Spinal cord syndromes

Complete cord syndrome: Loss of all motor, sensory and
autonomic functions below the level of injury
Anterior cord syndrome: anterior corticospinal tract injury à
motor affection mainly in the lower limbs.
Posterior cord syndrome: dorsal column injury, affection of

proprioception and vibration sense
Central cord syndrome:

• Weakness affecting mainly the upper limbs more than the
lower limbs (because the fibers of the upper limbs are more
medial within the cord than those of the lower limb)
• Weakness affecting the proximal group of muscles more than
the distal one. (Because the fibers supplying the proximal
group of muscles are more medial within the cord than those
supplying distal group of muscles)
51
Cord hemi section (Brown-Sequard syndrome):
On the same side:
-‐ At the level of the lesion: Loss of motor function due to affection of
the anterior horn cells (leading to lower motor neuron lesion) and
loss of sensory function due to affection of the posterior horn cells.
-‐ Below the level lesion: Motor paralysis (corticospinal tract) and loss
of prorioception and vibration sense (posterior column).
On the contralateral side:
-‐ Loss of pain and temperature sensation below the level of the lesion.
(lateral spinothalamic tract).
Types of motor neuron lesion due to cord compression

[SPINAL CORD COMPRESSION] 53
UMNL LMNL
Paralysis Below the level of the lesion At the level of the lesion
Muscle state Minimal wasting Maximal wasting
Tone Increased Decreased
Clonus Present Absent
Fasciculation Absent Present
Reflexes
1. Deep Hyperreflexia Hyporeflexia

2. Superficial Absent Present
Abdominal
Plantar Extensor (+ve Babiniski) Flexor or absent
Sphincters Urgency and automatic urinary Retention with overflow,

bladder (spastic bladder) hypotonic bladder (flaccid
bladder)
53
Spinal fracture
Epidemiology:
-‐ More common in males.
-‐ More common in 2nd and 3rd decades.
N.B.: - fracture of the spine is rare in children due to laxity of the

ligaments however spinal cord injury can occur. Spinal cord injury without
fracture can occur also in old age in the cervical region when there is
preexisting cervical canal stenosis.
Etiology:
-‐ Road traffic accidents.
-‐ Falling from height.
-‐ Sport injuries as diving injuries, horse riding, cycling injuries etc.
Mechanisms of: spinal injury:

-‐ Flexion: e.g. seat belt (dorsal spine injury), diving (cervical spine injury).
-‐ Extension: e.g. road traffic accident.
-‐ Torsion: e.g. sport injuries.
-‐ Compression: e.g. falling from height while standing or sitting.
-‐ Distraction: e.g. during hanging (distraction and extension).
[SPINAL FRACTURE] 55
Pathology:
Trauma to the spine can lead to various degrees of injury to the vertebral column
and/or the neural structures.
Vertebral column injuries:
1- Bony injuries e.g. fracture of the vertebral body, lamina, spinous

process, transverse process etc.
2- Ligamentous injuries or disc injuries.
Most common bony injuries:

o Burst fracture: when there is disruption of the upper end
plate or the lower end plate or both.
o Wedge fracture: no disruption of the end plates but there

is decrease in height of the anterior border of the vertebral
body
55
Assessment of bony instability:
The spine is divided into 3 columns: anterior, middle and posterior. More than
one column affection leads to instability.
Cord and root injuries:
Spinal cord: ranging from neuropraxia, edema, or compression by

bone, contusion, laceration or complete cord transsection.
Nerve roots: ranging from neuropraxia, edema, compression by

bone, contusion, laceration or complete avulsion of the root .
Spinal shock: refers to either:
I. Vascular shock: patients with spinal cord injuries may be

hypotensive due to the following factors:
i. Blood loss due to associated injuries.
ii. Loss of muscle tone in the lower half of the body will lead to
decrease in the venous return and decrease cardiac
output resulting in hypotension.
iii. Interruption of the sympathetic tone to the heart will result in
bradycardia, and will cause vasodilatation to the blood vessels
II. Neurologic shock: transient loss of neurological functions

below the level of the injury, on examination there will be loss of
voluntary movements however there will be sacral sparing (persistent
anal tone, positive bulboanal reflex, voluntary big toe movements).
[SPINAL FRACTURE] 57
Clinical picture:
Those due to trauma of the spine:
-‐ Pain especially on movements.

-‐ Tenderness.
-‐ Muscle spasm.
-‐ Contusion of the back of the neck.
-‐ Deformity.
Those due to neurological injury:
-‐ The patient may be intact.

-‐ Different degrees of weakness in the lower limbs (in case of dorsal
spinal cord injury) or in both upper limbs and lower limbs (in case of
cervical cord injury).
-‐ Sphincteric disturbances.
-‐ Respiratory difficulty (the higher the lesion the more the respiratory
difficulty).
According to the site of cord injury, the patient will manifest with one of the
cord syndromes mentioned in he previous chapter
Management:
Initial management:
-‐ ABC: (Airway, Breathing and Circulation).
-‐ Transfer of the patient:
If there is suspicion of spine fracture (e.g. weakness, tenderness,
major trauma etc.)
Cervical: neck collar
Dorsal or lumbar: transportation on a hard board.
Hospital management:
Radiological investigations:
-‐ Plain-Xray of the whole spine for a screening purpose (to diagnose and
identify the site of spine fracture).
-‐ C.T. scan: best for identification of bony details.
-‐ MRI : best for identification of soft tissue details ( disc , ligaments , spinal
cord )
57
Medical treatment:
-‐ Not an alternative to surgery if surgery is indicated.

-‐ In the form of bed rest, analgesics and methyl prednisolone.
-‐ Methyl prednisolone should be given in the first 6 hours after trauma.
Surgical treatment:
General principles for surgery:
a- In case of neural compression:

Surgical decompression in the form of laminectomy,
foraminotomy, excision of a retropulsed bone fragment from the
vertebral body that compress neural structures.
b- In case of vertebral column instability:
Stabilization by screws and plates or rods either by anterior or
posterior approach, in addition the bone yield during surgery is put
in a fashion to do further stabilization after bony fusion.
c- In case of deformity:
Reduction of deformity: preoperative (only in case of cervical spine
injury by the so called cervical traction) or intraoperative correction
of the deformity.
d- The surgery should be always directed towards the pathology
e.g. in case of traumatic cervical disc prolapse and instability:
cervical discectomy and fixation is done
e- In case of complete spinal cord transection, the fixation of an
unstable spine is beneficial to allow patient rehabilitation (with
a fixed spine the patient can sit on a wheel chair) and for
psychological aspect.
[DEGENERATIVE SPINAL DISORDERS] 59
Degenerative spinal disorders
Cervical disc prolapse

Anatomy
Inter vertebral disc consists of:
1. Two cartilaginous end plates.

2. Nucleus pulposus: softer form of cartilage
3. Annulus fibrosus: concentric layers of fibrous tissue and fibrocartilage
Pathophysiology
• Cervical disc prolapse occurs when the soft nucleus pulposus herniates
through tear in the annulus (peripheral fibrous cartilage). This may result from
a single or from repeated incidence.
• The cervical spine exhibits a great deal of mobility but little weight bearing
function.
• The intervertebral discs serve as mechanical buffers that absorb axial

loading, bending and shear forces.
Site
Cervical disc prolapse more common in C5-C6 and C6-C7 levels
59
Clinical picture
The prolapse is usually posterolateral and causes root compression

(Radiculopathy).
If the prolapse is central it will cause cord compression (Myelopathy).
In case of root and cord compression Radiculomyelopathy occurs.
Symptoms:
• Neck pain and stiffness.
• Pain radiating down the arm and hand (brachialgia) exacerbated by neck
motion (extension).
• Paresthesia, tingling and numbness along the affected dermatome.
• Motor weakness
• Sphincteric dysfunction.
Signs:
Signs of Radiculopathy: depends on which root is compressed
Level C3-C4 C4-C5 C5-C6 C6-C7 C7-D1
Root C4 C5 C6 C7 C8
compressed
Sensory loss C4 C5 C6 C7 C8
Motor deficit Diaphragm Deltoid Biceps Triceps Hand
muscles
Reflex lost Biceps and triceps
brachioradialis
Signs of myelopathy: (cord compression)
- Spastic quadriparesis
- Hyperreflexia below the level of the compression
- Clumsiness and ataxia of the extremities
- Gait disturbance
- Sphincteric disturbance.
Investigations:
1. Plain x ray:
a. Loss of lordosis.
b. Narrowing of the disc space.
c. Osteophytes.
2. MRI: the best diagnostic technique.
MRI Cervical spine: C6-7 disc prolapse

3. CT scan
4. Myelography: not commonly used
61
Management
Either conservative or surgical
a. Conservative
Symptoms relevant to radiculopathy usually respond to conservative measures

as:
- Bed rest
- Avoidance of heavy lifting
- Physical therapy
- Analgesics
- Muscle relaxant
- Neck collar
b. Surgical
Indications for surgery:
1. Brachialgia not responding to medical treatment.

2. Progressive neurological deficit due to root compression.
3. Manifestations of cord compression i.e. myelopathy.
Surgical procedures include:
1. Anterior cervical discectomy.

2. Posterior cervical laminectomy with or without foraminotomy
Cervical spondylosis
• It is a degenerative change including vertebral bodies, neural arches, facet

joints, ligaments and blood vessels, which may or may not cause neurological
manifestations.
• Reduction of the sagittal diameter of spinal canal (less than 12 mm) can be
associated with cord compression leading to myelopathy.
Clinical picture
• Insidious onset.
• Radiculopathy, myelopathy or radiculomyelopathy
• Spastic weakness of the lower limbs, with clonus, and +ve Babiniski sign.
• Weak hand grip and clumsiness.
• Hypoalgesia due to spinothalamic tract affection.
Investigations
• Plain x-ray cervical spine.
• CT scan
• MRI is the most accurate
Management:
Conservative: as in cervical disc prolapse if there is no cord compression

Surgical:
• Posterior laminectomy with or without foraminotomy
• Anterior: Multilevel discectomy, removal of osteophytes and Stabilization
by interbody fusion or instrumentation.
63
Lumbar disc prolapse

Anatomy
Inter vertebral disc consists of:

1. Two cartilaginous end plates.
2. Nucleus pulposus (softer form of cartilage).
3. Annulus fibrosus (concentric layers of fibrous tissue and fibrocartilage).
Pathophysiology
• Lumbar disc prolapse occurs when the soft nucleus pulposus herniates
through tear in the annulus (peripheral fibrous cartilage). This may result
from a single or from repeated incidence.
• Lumbar disc prolapse is the cause of 90% of sciatica.
• There is history of falling or lifting heavy weights preceding the onset of

symptoms.
Site
The majority of LDP occurs at L4-L5 and L5-S1 (95%).
Clinical picture
The typical patient with acute lumbar disc prolapse is from 30- 50 years of
age in the most productive period of his life; and has complained of
chronic low back pain for some time prior to the onset of acute disorder.
- Herniation occurs either centrally or lateral.
- When laterally, it compresses the adjacent nerve root à (Radiculopathy).
- When central, it compresses the cauda equina à(Cauda-equine

syndrome).
Symptoms
- Back pain
- Sciatica (Pain in the leg in the distribution of the affected root) aggravated
by coughing and sneezing.
- Pain relief upon flexion of knee and thigh
- Numbness or tingling occurs in the distribution of the affected root.
- Motor weakness
- Bladder symptoms (urgency, frequency, retention)
Signs
A. Back signs:
§ Restricted spinal movement.
§ Local tenderness.
§ Scoliosis.
§ Paravertebral muscle spasm.
§ Obliteration of lumbar lordosis.
B. Signs of radiculopathy:
§ Motor weakness
§ Dermatomal sensory changes
§ Reflex changes
§
Radiculopathy depends upon the root compressed.
Level of disc L3-L4 L4-L5 L5-S1

prolapse
Compressed root L4 root L5 root S1 root
Motor weakness Quadriceps Dorsiflexors of Planterflexors of

the foot the foot
Sensory Medial part of the Lateral side of the Posterior part of
impairment calf, medial calf and dorsum the calf , lateral
malleolus and of the foot and malleolus, lateral
medial foot big toe foot and sole
reflexes Impaired knee Impaired ankle

jerk jerk
C. Clinical tests (nerve root tension signs):

• Straight leg raising test (SLRT): Passive elevation of the fully extended leg
is considered positive if the patients feels sciatica at an angle <60o. It is
+ve in lower disc prolapse (L5 and S1 root irritation).
• Femoral stretch test (reverse SLRT): with patient in prone position,
extends the hip joint. The patient feels a femoral pain. It is +ve in higher
disc prolapse (L2, L3 or L4 root irritation)
D. Neurogenic claudication: It occurs in cases of lumbar canal stenosis

E. Cauda equine
65
Cauda equina syndrome:
Presentation:
- Low back pain and bilateral sciatica
- Motor (LMNL): bilateral weakness of dorsi and plantar flexion of the

foot. Weakness of hip flexor and/or extensors and weakness of knee
flexors and/or extensors may also occur.
- Sensory: hyposthesia bilaterally according to the spinal roots affected

and saddle shaped hyposthesia.
- Reflexes: ankle reflex is lost bilaterally and also may be the knee reflex.
- Autonomic: sexual dysfunction (impotence), sphincteric disturbance

(retention or incontinence of urine, chronic constipation or incontinence
of stools, diminished anal tone).
- Clinical test: SLRT: positive bilaterally
Investigations:
Plain x ray:
• AP and lateral views
• Dynamic study (neutral, flexion, extension)
o Narrowing of the disc space.
o Osteophytes
o Obliteration of lumbar lordosis
o Scoliosis
o To exclude other pathologies as metastatic lesions.

CT scan: It detects lumbar canal stenosis; hypertrophied facet joint, and

narrow canal dimension.
67
MRI: the best diagnostic method in lumbar disc prolapse
Myelography: not commonly used nowadays as the MRI replaces it. It

outline the thecal sac as well as the nerve root in A-P, lateral, and oblique views.
Disc prolapse causes a filling defect in the theca and obliteration or displacement
of nerve root sleeve of the affected disc level or complete block of the dye.
Nerve conduction velocity and EMG : It will yield precise information

on root lesion.
Treatment:
Conservative treatment:
1. Bed rest for 2-4 days on hard board mattress.

2. Activity modification and avoid lifting heavy weights.
3. Exercise
4. Analgesics
5. Muscle relaxants
6. Reduction of body weight
7. Health education
Surgical treatment:
Indications:
1. Failure of non-surgical treatment.

2. Patients who do not want to invest time in a trial of non-surgical
treatment.
3. Urgent surgery:
- Cauda equina syndrome.
- Progressive motor deficit.
- Severe, unremitting, leg pain which is not relieved by
conservative measures.
Methods of surgical treatment:
Transcanal approaches:
a. Standard open laminectomy and discectomy

b. Microdiscectomy
c. Endoscopic discectomy
Intradiscal procedures in selected patients
a. Automated percutaneous lumbar discectomy (nucleotome)

b. Percutaneous endoscopic discectomy
c. Laser disc decompression
d. Chemonucleolysis
69
Lumbar canal stenosis

Types:
Congenital: congenital narrowing of the lumbar spinal canal.
Acquired: Spondylosis develops as a result of disc degeneration with
age. The disc space collapse, producing excessive strain on facet joint;
this in turn leads to their degeneration and hypertrophy.
o Predispose to root and cauda equina compression from a

prolapsed disc, osteophytes, thickened ligamentum flavum or
hypertrophied facet joint.
o Congenital narrowing of the spinal canal aggravates the effect of
nerve root and/or cauda equina compression.
Clinical picture
• Root pain and sense of heaviness of both lower limbs develops after
standing or walking, relieved by sitting or lying down (claudicating
sciatica).
• Neurological deficit, such as muscle weakness or sensory troubles are

bilateral, predominantly at one side.
• In many cases, sphincteric function impairment maybe manifested
Management
• Plain x ray may suggest lumbar spinal stenosis, but CT scan and MRI are
required to establish the diagnosis.
• Surgical treatment: wide laminectomy and root decompression.

Facetectomy may be done in some cases.
Lumbar spondylolithesis
• Forward sliding of one vertebral body over the other.
• This usually occurs between L5- S1 and L4-L5.
• Displacement is due to congenital defective facet articulation; fracture pars

inter articularis (isthmic spondylolisthesis) or prolonged degenerative
process of the spine (degenerative spondylolisthesis).
• Narrowing of the spinal canal may cause root compression.
Treatment:
Conservative:
1. External spinal support.
2. Analgesics.
3. Weight reduction.
Surgical:
Includes decompression and fusion of the involved levels. i.e. bony fusion
with rods and transpedicular screws.
Plain X-ray lumbosacral: showing L5-S1 fixation using screws and rods, with and
intervertebral cage for interbody fusion
71
Brain tumors
Overview
Primary brain tumors occur in approximately 6 persons per 100,000 per year.
Fewer patients with metastatic tumors reach a neurosurgical center, it is
estimated that 25% of patients with a malignancy have a CNS metastasis. About
1 in 12 primary brain tumors occur in children under 15 years of age.
In adults the commonest tumors are gliomas, metastasis and meningiomas and
most of them lie in the supratentorial compartment.
In children the commonest tumors are medulloblastoma, cerebellar astrocytomas

and craniopharyngiomas.
Intracranial tumors are often described as “benign” or “ malignant”, but these

terms cannot be directly compared with extracranial counterparts:
-‐ Benign tumors: may have devastating effects if allowed to expand within
the rigid confines if the skull cavity. A benign astrocytoma may invade
widely through out the brain tissue preventing complete removal, or may
occupy a functionally critical site preventing even partial removal
-‐ Malignant tumors: implies rapid growth, poor differentiation, increased

cellularity, mitosis, necrosis and vascular proliferation, but metastases to
extracranial sites rarely occur.
WHO Classification of CNS tumors:
1. Tumors of neuroepithelial tissue

2. Tumors of cranial & spinal nerves as schwanomma or neurofibroma
3. Tumors of the meninges
4. Hematopoietic neoplasms as primary CNS lymphoma or plasmacytoma
5. Germ cell tumors
6. Cysts and tumor-like lesions
7. Local extension from regional tumors as: paraganglioma (glomus jugulare
tumor), chordoma and nasopharyngeal carcinoma
8. Metastasis
[BRAIN TUMORS] 73
Tumors of neuroepithelial tissue
Subdivided into
a) Astrocytoma: arise from astrocytes and represent the most primary
intra-axial brain tumor. Based on histopathological criteria, they could
be classified into 4 grades with WHO Grade 1 being the most benign
and WHO grade 4 (also known as glioblastoma multiforme) being the
most malignant.
b) Oligodendroglioma: arise from oligoendrocytes that normally form the

myelin sheath in the white matter.
c) Ependymoma: arise from the ependymal lining of the ventricles
d) Mixed tumors as oligoastrocytoma
e) Choroid plexus tumors as choroid plexus papilloma
f) Pineal tumors as pineocytoma
g) Enlarged tumors as primitive neuroectodermal tumors (PNET)
73
Tumors of the meninges:
Arise mostly from the arachnoid cap cells. Meningiomas are mostly benign
tumors but sporadic cases of aggressive meningiomas may occur. The
later group is subdivided into atypical meningioma (WHO grade 2 ) or
anaplastice meningioma (WHO grade 3)
Meningioma is considered an extra-axial tumor as they arise from the
meninges not from the brain tissue.
Germ cell tumors

They usually occur in the midline especially in the pineal region or the
suprasellar region. They include different types of tumors as:
-‐ Germinoma
-‐ Teratoma
-‐ Embryonal cell carcinoma.
Some of these tumors respond very well to radiotherapy.
Cysts and tumor like conditions

These are not true tumor but the represent space occupying lesions
mimicking the clinical picture of brain tumors as:
-‐ Dermoid cyst

-‐ Colloid cyst of the third ventricle
[BRAIN TUMORS] 75
Pituitary tumors:
Pituitary adenoma arises primarily from the anterior pituitary gland They
are classified according to the size into microadenoma (diameter less than
1 cm) and macroadenoma (diameter is greater than 1 cm) or according to
endocrinal function into hormone secreting or non-secreting adenoma.
Pituitary adenoma usually grows upward compressing the optic chiasm

causing bitemporal hemianopia. If the tumor grows further upward, it can
compress the 3rd ventricle and hypothalamus causing obstructive
hydrocephalus and hypothalamic manifestations. Less commonly, pituitary
adenoma can grow laterally into the cavernous sinus leading to
compression of the 3rd, 4th and 6th cranial nerves and cause strabismus or
ophthalmoplegia.
Hormone-secreting adenomas include
-‐ Growth hormone secreting adenoma (usually macroadenoma): cause

gigantism (before puberty) or acromegaly (after puberty)
-‐ Prolactinoma (usually macroadenoma): amenorrhea, glactorrhea

syndrome in women. Impotence and gynecomastia in men and infertility in
both sexes.
-‐ ACTH (usually micoradenoma) secreting adenoma: Cushing’s disease
-‐ TSH secreting adenoma: very rare and cause secondary thyrotoxicosis.
-‐ Rarely the tumor may secrete several hormones at the same time.
Craniopharyngioma:
It arises from embryonic remnants of Rathke’s cleft present in the pituitary stalk.
It is a benign tumor, which usually contains cysts and areas of calcification.
Similar to pituitary adenoma, craniopharyngioma exerts sometimes-mechanical
compression on the visual pathway and the 3rd ventricle. Pituitary hypofunction
and diabetes inspidus are commonly associated due to pituitary stalk
compression. Craniopharyngioma is commonly found in children and young
adolescents
75
Medulloblastoma
Considered one of the primitive neuroectodermal tumors (PNET). It is the most

common malignant pediatric brain tumor and the most common PNET. It usually
arises from the roof of the fourth ventricle producing obstructive hydrocephalus.
10 – 35% of cases develop spinal metastasis (drop metastasis) via CSF.
Clinical Picture of brain tumors
General manifestations include manifestations of increased intracranial

pressure (ICP): headache, blurring of vision, nausea, projectile vomiting and
seizures
Regional manifestations
Depend on the site of the tumor.
Frontal lobe tumor

• Contralateral face, arm or leg weakness
• Expressive dysphasia (dominant hemisphere)
• Personality changes:
i. Antisocial behavior
ii. Loss of inhibitions
iii. Intellectual impairment
iv. Profound dementia especially if the corpus cullosum is
involved
Parietal lobe tumors

• Disturbed cortical sensation
i. Tactile localization
ii. Two point discrimination
iii. Asteroegnosis
iv. Sensory inattention
• Visual field defect: lower homonymous hemianopia
• In dominant hemisphere:
i. Right/left confusion
ii. Finger agnosia
iii. Acalculia
iv. Agraphia
• Non dominant hemisphere:
i. Sensory or motor hemineglect syndrome
[BRAIN TUMORS] 77
Temporal lobe tumors:

• Psychomotor epilepsy
• Receptive dysphasia (dominant hemisphere).
• Visual defect: upper homonymous quadratanopia
Occipital lobe tumors: visual field defect (homonymous hemianopia),

visual hallucination and cortical blindness.
Supra sellar tumors as pituitary adenoma and craniopharyngioma:

bitemporal hemianopia, hormonal dysfuntion (vida supra) and hypothalamic
manifestations.
Tumors affecting Corpus cullosum Interhemispheric disconnection

syndrome
• Left side apraxia
• Pure word blindness or alexia without agraphia
Posterior fossa tumors: obstructive hydrocephalus due to obstruction of

the 4th ventricle and cerebellar manifestations as tremors, ataxia, dysmetria and
nystagmus.
Cerbellopontine angle tumors: as acoustic shwannoma; cerebellar

manifestations and cranial nerve dysfunction:
• Trigeminal: facial hypothesia, neuralgia, loss of corneal reflex.

• Facial: facial palsy
• Vestibulochochlear: tinnitus and sensory neural hearing loss
• Lower cranial nerves: difficult swallowing, loss of gag reflex and
frequent aspiration
77
Investigations
Radiological investigations
MRI brain with GAD (gadolinium): the golden diagnostic tool as it defines
clearly the tumor extension and its relation to the surrounding structures.
It shows:
-‐ Site
-‐ Mass effect
-‐ Lesion multiplicity
Axial, coronal and sagittal scanning provide valuable information about the
exact anatomical relationship of the tumor to the sulci and gyri, the
ventricles, the falx and tentorium cerbelli.
IV gadolinium provides a paramagnetic enhancement that increases

sensitivity of detection and clarifies the site of origin i.e. intrinsic or
extrinsic, and may delineate the border between tumor and surrounding
oedema.
CT brain with contrast: superior to the MRI in the delineation of bony

structures and/or tumor calcification as in oligodendroglioma, craniopharyngioma
and calcified meningioma
Angiography: to study the vascularity of the tumor and its relationship with
important vascular structures.
Plain x-ray:
a. Calcification as in oligodendroglioma, craniopharyngioma.

b. Osteollytic lesions in primary or secondary bone tumors,
Chordomas
c. Erosion of the posterior clinoids from local pressure as in
cranipharyngioma
d. Ballooning of the sella in large pituitary adenoma.
e. Pineal shift: seen if the gland is calcified
SPECT and PET scan: helps identify high-grade activity within a tumor.
Useful to exclude if proposing conservative management or in planning
stereotactic biopsy
[BRAIN TUMORS] 79
Laboratory investigations
1- Routine investigations
2- Hormonal assay: for pituitary adenomas, craniopharyngiomas or any
tumor compressing the pituitary stalk.
3- Tumor markers: important with germ cell tumors e.g. α-fetoprotein
4- CSF analysis: lumber puncture is contraindicated if the clinician suspects
an intracranial tumor. If CSF is obtained by another source e,g ventricular
drainage or during shunt insertion, then cytological examination may
reveal tumor cells
Lines of treatment of brain tumors:
Surgical excision
It is considered cornerstone in the treatment of brain tumors, especially, in

large sized tumors. It is usually performed through a craniotomy flap but in
certain cases other routes could be attempted as transsphenoidal approach
for pituitary tumors.
Biopsy
Used sometimes to establish diagnosis in controversial cases. Biopsy can
be done using standard microsurgical techniques (through a small craniotomy
flap) or by stereotaxy especially in deeply seated lesions.
Conventional Radiotherapy
Used either as a substitute for surgery in medically unfit patients and in
some inoperable tumors or as an adjuvant treatment after surgery in case of
malignant tumors or in the presence of residual tumor.
Stereotactic Radiosurgery
Multiple converging beams from a linear accelerator, gamma knife or
cyberknife, are focused on a selected target in a single treatment.
Proton Beam therapy

It is available only in few centers. It allows the delivery of high doses of
radiation to a very localized region adjacent to vital structures such as skull base.
79
Chemotherapy
Example: temozolomide, an oral alkylating agent that is used in the treatment or
relapsed anaplastic astrocytoma and newly diagnosed Glioblastoma multiforme.
Medical treatment:
-‐ Medical dehydrating measures can be used before or during surgery to

decrease the intracranial pressure.
o Steroid therapy: it dramatically reduce odema surrounding intracranial
tumors. It do not affect the tumour growth
-‐ Antiepileptic drugs are also needed to prevent epileptic fits in patients with brain
tumors.
-‐ Medical treatment is of utmost importance in the management of functioning
pituitary adenomas especially in prolactinoma, which can be treated medically
using dopamine agonist as bromocriptine or cabergoline.
[CEREBRAL ABSCESS] 81
Cerebral abscess
Epidemiology
Approx. 1500 – 2500 cases per year in the US, Incidence is higher in developing
countries
Risk factors
- Pulmonary abnormalities
o Infection
o AV fistulas
- Congenital cyanotic hearty disease
- Bacterial endocarditis
- Penetrating head trauma
- Chronic sinusitis/ otitis media
- AIDS
Sources of infection
Hematogenous
Abscesses are multiple in 10 – 50% of cases. No source can be found in 25% of
the cases. Chest is the most common origin.
Contiguous
- From purulent sinusitis/ middle ear infection: spreads by local
osteomyelitis or phelibitis of the emissary veins
o Middle ear and mastoid air sinus infection à temporal lobe and
cerebellar abscess
o Ethmoid and frontal sinusitis à frontal lob abscess.
o Sphenoid sinusitis: the least commonà cavernous sinus
thrombosis and temporal lobe abcesss
Following penetrating cranial trauma or neurosurgical procedure
Pathogens
1. Cultures from cerebral abscesses are sterile in up to 25% of cases
2. In general: Streptococcus is the most frequent organism
3. Multiple organisms may be cultured to varying degrees
81
4. Post traumatic and following neurosurgical procedures is usually due to

Staph. Aureus or Enterobacteriaceae
5. Fungal infections are more common in immune-compromised patients.
6. Infants: gram negatives are more common.
Presentation
Non are specific for abscess and many are due to edema surrounding the lesion,
symptoms tend to progress more rapidly than with neoplasms:
- Increased ICP (headache, nausea and vomiting, lethargy)

- Neurological deficit according to the site of the lesion with hemiparesis
and seizure in 30 – 50% of the cases.
- Presentation in newborns: cranial enlargement, seizures, irritability, failure
to thrive, and meningitis.
Evaluation:
Lab investigations
- Peripheral WBC: may be normal or mildly elevated in 60 – 70% of the

cases (usually > 10,000)
- Blood culture: should be obtained when abscess is suspected
- ESR: may be normal (especially in congenital cyanotic heart disease
when polycythemia lowers the ESR)
- CRP: Elevated. Sensitivity is 90% and specificity is 77% (maybe elevated
in noninfectious inflammatory conditions and brain tumors)
Brain imaging
- CT: ring enhancing. Sensitivity = 100%

- MRI: according to stage:
o Cerebritis: hypointense in T1 and high signal in T2
o Capsular:
§ Lesion center: low signal
§ Capsule: mildly hyper intense
§ Perilesional edema: low signal
[CEREBRAL ABSCESS] 83
Staging of cerebral abscess:

Stage Histologic characteristics Resistance to aspirating needle
1 Early cerebritis: (days 1- 3) Intermediate resistance
early infection and inflammation,
poorly demarcated from the
surrounding brain, toxic changes
in neurons, perivascular
infiltrates
2 Late cerebritis: (days 4- 9) No resistance
reticular matrix (collagen
precursor) and developing
necrotic center
3 Early capsule: (days 10 – 13) No resistance
neovascularity, necrotic center,
reticular network surrounds.
4 Late capsule: (> day 14) Firm resistance, “pop” on entering
collagen capsule, necrotic
center, gliosis around capsule
Treatment
Usually involves surgical drainage or excision, correction of the primary source

and long-term use of antibiotics (IV X 6-8 weeks followed by oral route for 4-8
weeks).
Medical treatment:
In general, surgical drainage or excision is employed in the treatment. Purely

medical treatment of early abscess (cerebritis stage) is controversial.
It includes:
• Antibiotics
o Initial antibiotics should be chosen according to the suspected
pathogen. E.g in history of trauma or neurological procedure, Staph
aureus is suspected and vancomycin should be initiated
o Change the type of antibiotic according to culture and sensitivity.
o IV antibiotics should continue for 6 – 8 weeks followed by oral route
for 4 – 8 weeks.
• Anticonvulsants: in seizures and prophylactic use is optional.
83
• Steroids: reduces the surrounding edema however, its use is

controversial.
Surgical treatment:
Options:
1. Needle aspiration: the mainstay of surgical treatment.
2. Surgical excision: recommended in traumatic abscess to debride foreign

material and in fungal abscess because of antifungal resistance.
[CEREBROVASCULAR DISORDERS] 85
Cerebrovascular Disorders
I Stroke
Definition
Stroke by the World Health Organization (WHO) is defined as clinical symptoms

of focal and/or global disturbance of cerebral function lasting more than 24 hours
or leading to death, with no apparent cause other than vascular.
Stroke is one of the leading causes of permanent disability and is the third largest
cause of death in western countries. The etiology of stroke includes both cerebral
hemorrhage originated for example from cerebral aneurysm or brain AVM and
ischemic cerebral infarction results from occlusive disease of the extracranial or
major intracranial arteries (atherosclerotic lesions), and the majority of these
strokes (around 85%) are of ischemic origin.
85
Ischemic Stroke
Classification
Stroke classification is based on the origin or possible source of embolism,

usually divided into four different categories:
• Cardiac (eg atrial fibrillation),
• Large artery strokes (lesions in the aortic arch, extracranial vessels or the
major intracranial branches),
• Small vessel disease/lacunar infarctions (occlusion of Reversib

minor intracranial branches), le
ischemic
• Others (eg. carotid dissection or sinus thrombosis). neurologi
Clinical Presentation of Ischemic Stroke
These are classified into:
1-T.I.A. (Transient Ischemic Attacks): Episode which is sudden in onset,

resolve within 24 hours or less. It leaves no residual deficit.
2-R.I.N.D. (Reversible Ischemic Neurological Deficit): It lasts more than 24

hours, but resolve within one week.
3-Complete stroke: Typically, it results in profound multimodal neurologic

deficit. Such as: hemiplegia, hemisensory effect, and hemianopia.
A. Affecting the carotid territory:
• Reduction in retinal perfusion leading to transient monocular blindness

(Amourosis Fugax).
• Reduction in cerebral perfusion leading to hemiparesis, hemianaesthesia,

and dysphasia.
B. Affecting the vertebrobasilar territory:
• Binocular visual disturbance, diplopia, and nystagmus.
• Vertigo, ataxia, deafness, and tinnitus.
• Bilateral weakness, and may be loss of consciousness.
• In this type, there is transient ischemia of the brain stem, occipital lobes,
medial temporal lobes, and the upper spinal cord.
Imaging
Extracranial, intracranial carotid or middle cerebral artery stenosis can be

diagnosed and measured using different imaging modalities. The “golden
standard” used in the majority of the large randomized trials is digital subtraction
angiography (DSA). Other non-invasive modalities have been established such
as Magnetic Resonance Angiography (MRA), Computed Tomography
angiography (CTA).
87
CT brain showing right MCA infarct
MRI brain showing diffusion-perfusion missmatch

Digital subtraction angiography
Treatment
Stroke prevention is primarily based on medical treatment, but in some

situations surgical or endovascular treatment becomes the method of choice.
Medical treatment to reduce the overall risk includes antiplatelet medications,
statins (with several beneficial effects in addition to lowering lipids), and
anticoagulation for atrial fibrillation, smoking cessation, control of hypertension
and metabolic control in the diabetic patients.
Management for acute ischemic stroke:
• ABCs : (Airway, Breathing and Circulation)
• Labs: CBC/ Plt, coagulation profile, blood glucose level, lipid profile.
• ECG, Cardiac monitor
• Establish IV access
• Baseline vitals, most important BP, SBP must be less than 185/110 for the
acute intervention
• Exam/NIHSS
• Rule out hypoglycemia, Seizures
• Rule out hemorrhage or massive infarction by CT and if available CTA
• IV-tPA if no contraindication (intravenous plasminogen activator)
• Or endovascular treatment if IV-tPA is contraindicated
89
Management for extracranial, intracranial carotid or

middle cerebral artery stenosis:
Strategies for revascularization in patients with intracranial carotid or middle

cerebral artery stenosis include surgical bypass, percutaneous transluminal
angioplasty (PTA) alone, and percutaneous transluminal angioplasty and stenting
(PTAS). Revascularization by means of extracranial–intracranial bypass surgery
in stenotic intracranial arteries was shown to be inferior as compared with
medical therapy. Percutaneous balloon angioplasty has been reported in several
retrospective case series to be useful and safe for the treatment of stenotic
intracranial arteries, but still holds a risk of vascular dissection, elastic recoil,
vasospasm, and high-grade residual stenosis because of the small caliber of the
vessel.
Hemorrhagic stroke
Etiology:
1) HYPERTENSION (most common cause)
The most frequent sites of hypertensive intracerebral hemorrhage are the basal
ganglia and thalamus and less commonly, may involve the cerebellum, the pons
2) Lobar hematoma due to rupture of vessel within the brain parenchyma:
• Systemic coagulation disorders
• Amyloid deposits
• Vasculitis
• Saccular aneurysm
• Vascular malformations
Clinical Picture
• Abrupt severe headache and Vomiting followed by
• Rapid Decrease level of consciousness up to coma
• Specific neurological symptoms develop and is dependent on the

location:
§ Cerebrumà hemipariesis, hemisensory loss, 3rd nerve
palsyà tentorial herniation and coma
§ Cerebellum à ataxia, nystagmus, obstructive hydrocephalus
§ Pontineà sudden loss of consciouness, quadriplegia, pin
point pupils.
91
Investigations
• Routine, coagulation profile work up
• CT scan (Best for Intracranial hemorrhage) and MRI: Site, size, mass
effect, extent, associated pathologies
• Angiography (DSA, CTA,MRA) for the diagnosis of aneurysm and AVM.
Treatment
1) Hospitalization
2) ABC (Airway, Breathing and Circulation)
3) IV Fluids
4) Medical
• Control hypertension
• Control ICP
• Anticonvulsant
5) Surgical
• Craniotomy with evacuation of clot under direct vision + hemostasis
• Resection source of bleeding (AVM)
• Suprtentorial:
o Surgical evacuation If sizable, superficial, clinically
acceptable patient
o Conservative management if small, deep
• Cerebellar:
o Urgent evacuation, life saving as it reliefs brainstem
compression
• Pontine:
o High mortality à conservative management
II Aneurysms
Definition
Aneurysm may be defined as “an abnormal blood-filled dilatation of a blood
vessel resulting from a disease of the vessel wall” (1). Intracranial aneurysms are
common acquired lesions commonly located at the branching points of the major
intracranial arteries coursing through the subarachnoid space at the base of the
brain.
Prevalence
The estimated adult prevalence of intracranial aneurysms in large autopsy series
varies from 1% to 6% of the population.
Common sites for intracranial aneurysms
93
Clinical Presentation
Subarachnoid Hemorrhage
The typical presentation of aneurysmal subarachnoid hemorrhage is sudden
onset of severe headache, which may be associated with nausea, vomiting, and
meningeal irritation signs. The patient may lose consciousness. These meningeal
irritation signs include neck stiffness which usually develops several hours after
the hemorrhage, severe lower back pain and bilateral radicular leg pain due to
the subsequent circulation of bloody cerebrospinal fluid down the spinal axis.
Mass Effect
The most common clinical presentation due to mass effect of intracranial
aneurysms is third nerve palsy associated with carotid-posterior communicating
aneurysms. Some intracranial aneurysms often of the large or giant types
present with visual field defects, trigeminal pain, ophthalmoplegia, seizures, and
hypothalamic–pituitary dysfunction.
Cerebral Ischemia
Stroke may be the presenting clinical manifestation of an unruptured intracranial
aneurysm. Such ischemia is usually due to the detachment of an embolus from
an intra-aneurysmal thrombus, and it should be differentiated from intracranial
arterial dissection with the secondary formation of an aneurysm.
Asymptomatic Unruptured Intracranial Aneurysms

With the widespread use of helical (spiral) CT angiography and magnetic
resonance angiography, many unruptured asymptomatic intracranial aneurysms
can now be detected.
Diagnostic Imaging
CT scanning
Detects Subarachnoid hemorrhage. Very sensitive in detecting any associated

intracerebral hemorrhage or hydrocephalus. If there is a strong clinical suspicion
of a subarachnoid hemorrhage but the CT scan is normal, a lumbar puncture
should be performed to exclude the presence of xanthochromia in the CSF.
Conventional angiography
Conventional angiography and 3D angiography remains the gold standard for

detecting an intracranial aneurysm and determining its anatomical
characteristics.
95
MRI angiography
MRI angiography essentially carries no risk as it does not require the

intravascular administration of contrast material.
CT angiography
The detection rate with this technique is similar to that with MRI angiography.
Treatment
Complete anatomical exclusion of the aneurysm sac from the intracranial
circulation with parent artery preservation is the main treatment goal to prevent
future rupture or re-rupture with its devastating consequence. This aim can be
achieved either by open microneurosurgical clipping or endovascular
embolization.
III Brain arteriovenous malformations

(AVMs)
Definition
Brain AVMs are composed of a network of blood channels (nidus) supplied by
cerebral arterial feeders, drained by veins emptying into the venous sinuses, and
surrounded with gliotic non-functioning brain parenchyma.
Natural History
The risk of hemorrhage from a brain AVM has an average 2 to 4% yearly risk of
hemorrhage from brain AVM.
97
Clinical Presentation
Brain AVMs most commonly present with intracranial hemorrhage, other
presentation possibilities include headache, epilepsy, focal neurological deficit
not related to hemorrhage, or may be found incidentally during brain imaging
studies for other causes.
Intracranial Hemorrhage
The most common clinical presentation of brain AVM is intracranial hemorrhage.
Bleeding from brain AVMs can give rise to subarachnoidal hemorrhage,
intracerebral hematoma, and or intraventricular bleeding.
Epilepsy
Epilepsy could be the presenting symptom in 30% of patients with brain AVM. In
the majority of cases, seizures are partial or partial complex and sometimes with
secondary generalization type seizures. Cortical AVMs are more often result in
seizures than deep AVM.
Headache
Headache is the presenting symptom in approximately 30% of cases.
Focal Neurologic Deficits

Focal neurologic deficits may be progressive, stable, or reversible. Progressive
neurologic deficit may be the result of steal phenomenon, venous hypertension,
or mass effect.
Diagnostic Imaging
CT scan
CT scan mainly to rule out hemorrhage and if hyperdense serpiginous structures
are visible on contrast injection CT scan AVM is supected.
CT angiography
3D CT angiography provides good anatomic information on nidus and draining
veins. Small AVMs and small AVM feeders can be misdiagnosed by this
technique.
Magnetic Resonance Imaging

The brain AVM anatomical characteristics such as the size, location of the nidus,
and the proximity of the AVM nidus to eloquent brain regions are best defined on
magnetic resonance imaging (MRI) scans. In addition, MRI data clearly
demonstrate the status of the brain parenchyma surrounding the AVM, MRI
clearly defines areas of encephalomalacia or hemorrhage (recent or remote)
around the nidus, these data are very important for clinical correlation. Functional
MRI studies (fMRI) also are very helpful in detecting functional areas of the brain
particularly sensorimotor, visual, and language cortex and there relation to the
AVM.
Selective and Superselective Cerebral Angiography

The goals of superselective angiography are to assess the detailed anatomic
characteristics of the AVM, and to give an anatomical base for understanding the
nidal vascular compartmental angioarchitecture essential for embolization
planning.
Treatment
Treatment of brain AVMs should be done after a careful consideration of the
clinical data and AVM anatomy, potential risks must be carefully balanced
against the benefits in each patient . The treatment options available at the
present time for brain AVMs include:
• Surgical resection,
• Radiosurgery,
• Endovascular embolization: well-established treatment modality that is in

many circumstances included in the multidisciplinary approach for the
treatment.
99
Peripheral Nerve Disorders
Entrapment Neuropathy
Carpal Tunnel Syndrome
Carpal tunnel syndrome occurs as a result of compression of the median nerve

beneath the carpal transverse ligament, affects 1% of the population, and more
frequent in females.
The carpal tunnel syndrome should be considered when there is any unexplained
pain or sensory disturbance (e.g., intermittent numbness and pain of the hand
that is worse at night) and weakness of the abductor pollicis brevis, the lateral
two lumbricals, the opponens pollicis, and the flexor pollicis brevis muscles.
Contributing factors
Ligamentous or synovial thickening, Trauma, Obesity, Diabetes, Thyroid disease,
Amyloidosis, Gout, Acromegaly, Paget’s disease, Mucopolysaccharidoses
The following physical tests can be helpful in the diagnosis of carpal tunnel
syndrome.
Median nerve percussion test: The test is positive when tapping the area over the
median nerve at the wrist produces paresthesia in the median nerve distribution.
(Tinel's test).
Carpal tunnel compression test: The test is considered positive when the
patient’s sensory symptoms are duplicated after pressure is applied over the
carpal tunnel for 30 seconds.
Phalen wrist flexion test: This test is positive when full flexion of the wrist for 60
seconds produces the patient’s symptoms. Sensitivity 71%, specificity 80%
Electrodiagnostic tests: including Sensory conduction studies and

Electromyography: are the most sensitive physiological techniques for
diagnosing carpal tunnel syndrome.
[PERIPHERAL NERVE DISORDERS] 101
Differential diagnosis
• Cervical radiculopathy (C6, C7)

• Brachial plexopathy (Upper and lower plexus paralysis also Thoracic outlet
syndrome)
• Pronator teres syndrome due to compression of the median nerve
between the two heads of the pronator teres.
• Anterior interosseous syndrome:
Includes loss of flexion of the terminal phalanx of the thumb and the index
finger (pinch sign), and no sensory loss.
Management:
1- Treatment of the systemic disease.

2- Reduction of the hand usage.
3- NSAID
4- Division of the carpal transverse ligament in severe carpel tunnel
syndrome.
101
Ulnar Entrapment at the Elbow (Cubital tunnel

syndrome)
This results from entrapment of the ulnar nerve as it enters the forearm through
the narrow opening (the cubital tunnel) formed by the medial humeral epicondyl,
the medial collateral ligament of the joint, and the firm aponeurotic band, to which
the flexor carpi ulnaris is attached.
Elbow flexion reduces the size of the opening under the aponeurotic band, while
extension widens it.
Symptoms include paraesthesia, numbness, or pain in the fourth and fifth fingers,
occasionally provoked by prolonged elbow flexion, associated with decreased
vibratory perception and abnormal two-point discrimination.
Weakness affects the first dorsal interosseous muscle first and most severely.
Weakness and wasting of the hypothenar and intrinsic hand muscles result in the
loss of power. The sensory symptoms usually precede weakness.
Tinel’s sign may be present.
Electrodiagnostic tests: Motor nerve conduction velocity is important

for the diagnosing.
Management:
Neurolysis and decompression with or without ulnar nerve transposition.
Differential diagnosis
• Cervical radiculopathy (C8 –T1)

• Thoracic outlet syndrome, lower brachial plexopathy
• Syringomyelia
Dissociated sensory loss is characteristic, There are often associated long track
findings in the legs, and the MRI is diagnostic
• Motor neuron disease
There is weakness and wasting of intrinsic hand muscles. Thenar muscles as
well as the hypothenar muscles are often affected.
Fasciculations may be present, but the sensory disturbances are not found.
• Ulnar nerve entrapment at the wrist or hand (Guyon’s canal)
Includes sensory loss in the medial fourth and fifth fingers. The palmar and
dorsal surfaces of the hand are spared due to sensory nerve had branched
proximal to the wrist level.
Weakness is predominantly affecting ulnar-innervated thenar muscle relative to
the hypothenar muscles.
103
Meralgia Paresthetica
The lateral cutaneous nerve of the thigh is a purely sensory branch arising from
the lumbar plexus (L2–L3). It passes obliquely across the iliac muscle, and
enters the thigh under the lateral part of the inguinal ligament. It supplies the skin
over the anterolateral aspect of the thigh.
Numbness is the earliest and most common symptom. Patients also complain of
pain, paresthesias (tingling and burning) and often touch–pain–temperature
hypesthesia over the anterolateral aspect of the thigh.
The condition can also be due to:

- Obese individuals who wear constricting garments (e.g., belts, tight jeans,
corsets).
- Abdominal distension (as a result of ascites, pregnancy, tumor).
- Removal of an iliac crest bone graft if it is taken too close (2 cm) to the anterior
superior iliac spine.
Management:
– Weight reduction with NSAID

– Surgical neurolysis and decompression of the nerve where it passes
through its canal within the inguinal ligament.
–
Tarsal Tunnel Syndrome
This involves compression of the posterior tibial nerve at the ankle behind the
medial malleolus, where the laciniate ligament connecting the distal tibia to the
calcaneous covers it.
It is usually related to local fractures, tumors, and vascular abnormalities. The
entrapment results in hypoesthesia in the sole of the foot, a positive Tinel’s sign
with percussion, or pressure over the flexor retinaculum below the medial
malleolus.
Management
– NSAID with the conservative measures such as external ankle support
(e.g., shoe orthoses) to improve foot mechanics.
– Surgical release of the entrapment is not rewarding as often as in the
carpal tunnel syndrome.
105
Thoracic outlet syndrome
(cervicobrachial neurovascular compression

syndrome)
– The thoracic outlet syndrome may be purely vascular, purely neuropathic, or

rarely, mixed. The true neurogenic thoracic outlet syndrome occurs more
frequently in young women, and affecting the lower trunk of the brachial
plexus.
– Intermittent pain is the most common symptom, referred to the medial arm,
forearm and the ulnar border of the hand. Paresthesias and sensory losses
involve the same distribution.
– The motor and reflex findings are essentially those of lower brachial plexus
palsy, with particular involvement of the C8 root causing weakness and
wasting of the thenar muscles, similar to carpal tunnel syndrome.
– However, in contrast to the latter, in the thoracic outlet syndrome wasting
and paresis also tend to involve the hypothenar muscles.
– Electrodiagnostic studies show evidence of lower trunk brachial plexus
dysfunction.
– Plain X-ray: may show cervical rib.
– Angiography: may show vascular anomalies.
Management:
Includes removal of the cervical rib or sectioning of the fibrous band of the
anterior scalene muscle.
Traumatic Lesions
Pathology (types):
Concussion (Neuropraxia)
It is a transient neuronal physiological dysfunction, its function returns within 24-
48 hrs. It may occur with blunt injuries
Contusion (Axonotemesis):
• The epineuria and perineurium are totally intact.
• Alteration of the endoneurium (containing axons) occurs.
• All conductivity is lost in the distal segments.
• The axon distal to the site of injury degenerates (Wallerian degeneration).
• Such injuries occur after blunt trauma or penetrating trauma in the nerve
vicinity.
• Spontaneous regeneration may take place and the prognosis is good.
• Regeneration sometimes can't occur due to disruption of the fascicular
anatomy, but the nerve remains in gross continuity leading to the
formation of neuroma in continuity.
Complete disruption (Neurotemesis)

There is no possibility of regeneration without operative repair. It occurs in cut
and gun shot injuries and with fracture of long bones.
Types of traumatic agent:

• Cutting injuries: it is the most common cause of nerve injury, usually by
sharp instruments.
• Traction injuries
• Electric trauma: High voltage current may cause disruption of the nerve all
the way back to the anterior horn cell "AHC".
• Ischemic damage: Severe and prolonged compression may undergo
severe degeneration, e.g. plaster cast.
• Gunshot injury: It causes severe laceration of the nerve and difficulty in
approximation.
• Chemical injury
107
Upper Limb Nerves Injuries
1) Brachial Plexus Injury

Most commonly occurs as birth injuries.
Upper plexus (trunk) paralysis (Erb–Duchenne type)
– The muscles supplied by the C5 and C6 roots are paretic and atrophic (i.e.,
the deltoid, biceps, brachioradialis, radialis, and occasionally the
supraspinatus, infraspinatus and subscapularis muscles), producing a
characteristic limb position known as the “policeman’s tip” position (i.e.,
internal rotation and adduction of the arm, extension and pronation of the
forearm, and with the palm facing out and backward)
– The biceps and brachioradialis reflexes are depressed or absent.
– There may be some sensory loss over the deltoid muscle area.
Lower plexus (trunk) paralysis (Dejerine–Klumpke type)
– The muscles supplied by the C8 and T1 roots are paretic and possibly
atrophic (i.e., weakness of wrist and finger flexion and weakness of the small
hand muscles), producing a “claw-hand” deformity.
– The finger flexor reflex is depressed or absent.
– Sensation may be intact or lost over the medial arm, forearm, and ulnar
aspect of the hand.
– There is an ipsilateral Horner’s syndrome with injury of the T1 root.
109
Injuries in the axilla:
All major nerves of the upper limbs may be affected:
1. Musculocutanous nerve:
• There is weakness of the biceps and brachialis muscles and sensory
deficit in the lateral forearm.
2. Radial nerve:
• It affects all extensors of the elbow, wrist and fingers.
• Deformity: wrist and finger drop.
• Sensory loss: in the dorsum of the hand and the base of the thumb.
• Triceps reflex is lost.
3. Median nerve:
• There is weakness of the flexors of the fingers and opposition of the
thumb.
• Deformity: Ape hand deformity.
• Sensory loss: in the lateral 2/3 of the palm and the lateral three and half
fingers.
4. Ulnar nerve:
• There is weak flexion of the little finger, palmar and dorsal interossei. This
results in weak abduction and adduction of the fingers, and weak
adduction of the thumb.
• Deformity: partial claw hand deformity.
• Sensory loss: of the palmar and the dorsal aspect of the medial 1/3 of the
hand, and medial one and half fingers.
Injuries of the arm and the forearm:
Radial nerve in the spiral groove (lateral injury):
• There is wrist and finger drop with preservation of the elbow extensors.
• Sensory: loss of the dorsolateral aspect of the hand.
Posterior interosseus injury in the forearm:
Motor: paralysis of all extensors of fingers and most of the extensors of the wrist.
Deformity: finger drop only.
Sensory: no sensory loss.
Medial nerve injury (medial injury)
Deformity:
Pointing index deformity: due to paralysis of the flexor digitorum surperficialis

and the lateral half of the flexor digitorum profundus.
Ape-hand deformity: due to atrophy of the thenar muscles. Backward throwing

of the first metacarpus due to paralysis of the opponens pollicis muscle and over
action of the abductor pollicis longus => abduct the thumb.
Ulnar deviation of the hand
Atrophy of the flexor muscles, tips of the index and thumb, with or without skin
atrophic changes.
Special Motor Tests:
a) Pointing index test: Ask the patient to grasp his hands.

b) Radial grip of the hand is weak.
c) Pencil test (thumb abduction test): Abducting the thumb 90° from the
plane of the palm to test for the action of abductor pollicis brevis.
d) Weak pronation of the arm.
e) Opposition of the thumb across the palm fails.
Sensory System
Distribution: Lateral three and a half fingers on the palmar aspect and the
dorsum of the terminal phalanges.
111
Buttoning test: fails with closure of the eyes due to loss of deep sensation.
Ulnar nerve injury (medial injury)
Deformity
Partial claw hand: due to affection of the little and ring fingers only => flexion of
the interphalangeal joint, hyperextension of metacarpophalangeal joints of the
medial two fingers especially the little finger.
Radial deviation of the hand: due to paralysis of the flexor carpi ulnaris muscle.
Trophic changes: maximal on the tip of the little finger.
Atrophic changes:
• Sunken interossei spaces on the dorsum of the hand especially the first
space (most important).
• Atrophy of the hypothenar muscles and the tip of the little finger.
• Wasting of the muscles of the medial side of the forearm.
Specific Motor Tests
a) Weak ulnar grip.

b) Card board test: Abduction (dorsal interossei) and adduction (palmar
interossei) of the fingers fails; the patient is unable to hold a card in
between two fingers
c) Paper test: for the thumb to test for the action of the adductor pollicis
muscle. The patient will hold the paper by flexing the terminal phalanx
"Fromant's sign".
d) Flexion of the wrist shows radial deviation.
e) Abduction of the little finger fails.
Ulnar paradox
The higher the lesion of the ulnar nerve, the lesser the claw hand, because the
flexor digitorum profundus is completely paralyzed and no flexion of the
interphalanngeal joint takes place.
Sensory System
a. Lesions above 5 cm from the wrist: palmar and dorsal surfaces of the medial
one and half fingers and the medial third of the palm.
b. Lesions below 5 cm from the wrist: only the palmar surface is affected,
because the dorsal branch arises above that level.
c. Lesions below the wrist: have no sensory changes, because the superficial
branch escapes.
Wrist and hand injuries:
Median nerve injury:
Motor paralysis: of the thenar muscles and first and second lumbricals.
Deformity: Ape-hand.
Trophic changes: on the tip of the index finger
Atrophic changes: of the thenar muscles.
Tests: For abductor pollicis brevis muscle, the pencil test is used.
6. Sensory changes: Loss of sensation on the lateral three and half fingers,
dorsal nail beds and lateral half of the palm.
Ulnar nerve injury:
• Same motor affection as injury in the forearm, with the exception that the
partial claw hand is more severe (ulnar paradox)
• No sensory affection
113
Lower Extremities Injuries
Femoral nerve injury
– In wounds of the inguinal region.

– There is weakness of the quadriceps and knee extension muscles.
– Knee jerk is lost.
Sciatic nerve injury
The common peroneal nerve

– It is damaged by trauma to the fibular neck.
– Weakness of the dorsiflexors and evertors of the foot à foot drop.
– Sensory loss: over the dorsum of the foot.
The tibial nerve

– Weakness of the plantar flexors.
– Weak ankle jerk.
The Sciatic nerve

– It occurs in case of faulty IM injections and hip dislocation.
– Deformity: flail foot.
Management of traumatic nerve injuries

• In cases of neuropraxia or axonotemesis nerve regeneration is possible,
so operative repair is not required. It occurs usually after blunt trauma.
• Neurotemesis is an indication for surgery.
• Clean wounds can be repaired immediately (primary sutures).
• Crushed and contaminated wounds, nerve repair should be delayed for 3-
6 weeks (secondary sutures).
Advantages of secondary sutures:
1. Controlling infection.
2. Proper evaluation of the extent of injury.
3. Presence of an expert neurosurgeon and good operative room.
4. Have a thickened neurilemmal sheath that can withstand sutures.
5. Maximum rate of regeneration is after 3 weeks 1 ml/day.
NB:
Neurolysis is decided at the time of surgery.

Surgical microscope for nerve suturing is a must.
Strategies for management of nerve gaps include: Neurolysis, transposition,

flexion of the limb and autologous nerve graft (sural nerve).
The results of surgery depend on:

• Age: children give better results than adults.
• Duration: more than 3 months after injury have bad prognosis.
• Distance: between the site of injury and peripheral nerve (terminal
branches).
• Regeneration: 1-2 mm/day.
• Type of nerve: Pure motor or sensory nerves do better than mixed nerves.
• Care of the injured extremities is also important. And the joint should be
hold in functional position.
• Physical therapy is needed postoperatively.
115
Functional neurosurgery
Definition: The surgical destruction or chronic excitation of a part of the
nervous system as treatment of a physiological or psychological disorder.
The fields of neurosurgery where functional neurosurgery can be used

include:
1- Pain.
2- Involuntary movements.
3- Epilepsy.
4- Psychological disorders.
5- Spasticity.
Tools used in functional neurosurgery:
Conventional neurosurgical techniques: e.g. craniotomy,

laminectomy, etc.
Stereotactic procedures: Stereotaxy come from the Greek words

stereo mean solid and taxis means order. It is a technique where a device is
used to determine the exact three dimentional location of a point of the brain
along the X, Y and Z axes with the help of either the CT or MRI scanning.
Stereotactic device applied to the head and guiding a needle or a probe to a

specific target in the brain
The use of neural prosthesis: e.g. spinal cord stimulator, deep

brain stimulator, radiofrequency lesioning device, etc.
[FUNCTIONAL NEUROSURGERY] 117
Implanted spinal cord stimulator showing the pulse generator connected by

an extension to the electrodes through a lead wire
Implanted deep brain stimulator showing the pulse generator connected by an

extension to the electrodes that is inserted in the thalamus
117
;
Radiofrequency generator connected through a lead wire to the electrode
Radiosurgery:
It is a non-invasive procedure where beams of irradiation arising from a

specific device converge at a certain point in the brain causing lesion only at
this specific location and not injuring other parts of the brain.
shows the converging gamma rays in the target point, each ray is weak and does
not cause harm to the normal tissue, but when all the rays meet together at
specific point, they become strong enough to cause a lesion.
The use of functional neurosurgery for the

management of pain:
Cranial procedures:
Trigeminal neuralgia:
• Microvascular decompression of the trigeminal nerve through a
retrosigmoid approach where the compressing element (usually the
superior cerebellar artery) is separated from the trigeminal nerve.
• Percutaneous radiofrequency lesioning of the trigeminal nerve using a
probe connected to a radiofrequency generator under X-ray guidance
(using the C-arm). It is usually used when there is a contraindication for
surgery or if the patient refuses open surgery.
• Radiosurgery lesioning of the trigeminal nerve; a totally non-invasive
technique.
Other sources of pain:
• Intraventricular morphine infusion, usually in cancer pain.

• Bilateral cingulotomy, injury to the cingulated gyrus on the medial aspect
of the frontal lobe, using stereotactic or radiosurgical procedures.
Spinal procedures:
Low back pain:
• Facet joint denervation: where a percutaneous X-ray guided procedure

is used to coagulate the nerve of Luschka supplying the intervertebral
facet joint is done using the radiofrequeny generator thus abolishing pain
generated from the facet joints.
119
• Spinal cord stimulation:
A device known as spinal cord stimulator is used. It consists of a probe

inserted in the epidural space dorsally on the dorsal aspect of the spinal cord.
According to the gate theory of pain, electrically stimulating the dorsal column
of the spinal cord will abolish pain impulses in the spinal cord, thus relieving
pain. A test period to detect the efficacy of the stimulator is done first, if
proved effective, connection of the probe through leads to implantable pulse
generator is done and the battery of the generator can be changed every
several years.
• Insertion of morphine pump:
A catheter inserted epidurally or intrathecally and connected to a reservoir

can be used to infuse morphine at a special rate to relieve pain.
Sciatic pain, can be relieved at least temporarily by percutaneous X-ray

guided radiofrequency lesioning of the dorsal nerve root.
Deafferentiation and neuropathic pain: Results from

peripheral nerve injury e.g. brachial plexus injury, diabetic peripheral
neuropathy.
Procedures used include Drezz, where the dorsal root entry zone of the spinal
cord is coagulated using the radiofrequency generator.
Cancer pain:
Cordotomy:
Lesioning of the anterolateral quadrant of the cord interrupting the

ascending spinothalamic pain conducting pathway. It can be done either by
open surgery or percutaneously using radiofrequency generator.
Insertion of morphine pump.


management of involuntary movements:
Lesioning techniques:
Using a radiofrequency generator where a probe is introduced

stereotactically using CT or MRI guidance to a specific location.
Examples are:
Pallidotomy, where the globus pallidum interna is lesioned, used in

Parkinsonism and dystonia.
Thalamotomy, where the VIM (venteral intermedius nucleus) is lesioned,

used in Parkinsonism (especially for tremors) and in essential tremors.
Stimulation techniques using deep brain

stimulation:
The deep brain stimulator consists of a probe inserted in the desired

location in the brain, a lead connecting the probe to a pulse generator
inserted subcutaneously. It can be used in the following locations:
• The globus pallidus internus: in Parkinsonism

• The Vim of the thalamus, in parkinsonian tremors and in essential
tremors.
• In the subthalamic nucleus, in Parkinsonism.
Radiosurgery:
• Thalamotomy for parkinson’s disease and in essential tremors.

• Pallidotomy for parkinson’s disease
121

management of epilepsy:
Open surgery: examples include:
Temporal lobectomy: after confirming by EEG that the epileptic focus is in

the temporal lobe as in mesial temporal sclerosis.
Callosotomy, interrupting the crossing fibers in the corpus callosum, used in

generalized epilepsy.
Stimulation techniques:
Vagal nerve stimulation is used where a wire is wrapped around the vagus
nerve in the neck and connected by leads to an implanted stimulator.
Ascending impulses in the vagus nerve interrupts the abnormal electrical
activity that causes seizures.
Radiosurgery:
Lesioning the epileptic focus in mesial temporal sclerosis.

management of psychological disorders
(psychosurgery):
Using either lesioning techniques by a radiofrequency generator or
radiosurgery or stimulation techniques using a deep brain stimulator.
Commonly used targets for psychosurgery:
1- Anterior capsulotomy (the anterior limb of the internal capsule) in

depression and OCD (obsessive compulsive disorder).
2- Cingulotomy (lesioning of the cingulated gyrus on the medial side of the
frontal lobe) usually bilateral, in depression.
3- Subcaudate tractotomy, below the caudate nucleus, in OCD.

management of spasticity:
These procedures can be used in spasticity in cases of spinal cord injury

as well as in cerebral palsy.
1- Dorsal rhizotomy, where the dorsal rootlets of the spinal nerves are cut,
thus interrupting the afferent impulses from the muscles that cause efferent
impulses going back to the muscles increasing their tone causing spasticity.
2- Baclofen pump insertion:
Baclofen is a muscle relaxant acting at the spinal cord level. A pump is
inserted subcutaneously and connected to a small catheter that enters the
spinal subarachnoid space, infusing baclofen at a specific rate relieving
spasticity.
123

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[CONTENTS]

Types of Congenital Anomalies: 22

Scalp hematoma (cephalhematoma) 35

Diffuse axonal injury (DAI) 40

Management of head injuries 48

SPINAL CORD COMPRESSION 50

Mechanisms of: spinal injury 54

DEGENERATIVE SPINAL DISORDERS 59

Cervical disc prolapse 59

Lumbar disc prolapse 64

Cauda equina syndrome 66

Lumbar canal stenosis 70

WHO Classification of CNS tumors 72

Clinical Picture of brain tumors 76

Lines of treatment of brain tumors 79

Staging of cerebral abscess 83

Brain arteriovenous malformations (AVMs) 97

Focal Neurologic Deficits 98

PERIPHERAL NERVE DISORDERS 100

Entrapment Neuropathy 100

Traumatic Lesions 107

Upper Limb Nerves Injuries 108

Lower Extremities Injuries 114

Management of traumatic nerve injuries 115

FUNCTIONAL NEUROSURGERY 116

Tools used in functional neurosurgery 116

The use of functional neurosurgery for the management of pain 119

The use of functional neurosurgery for the management of epilepsy: 122

The use of functional neurosurgery for the management of psychological disorders

The use of functional neurosurgery for the management of spasticity: 123

Important in establishing the diagnosis, and must be taken in conjunction with

Lower Cranial nerves

Conscious level assessment

Area assessed Response Score

Eye opening Spontaneous 4

Higher cerebral function examination

- Dyphasia (listen to the patient’s language pattern)

o Receptive aphasia: fluent aphasia with impaired comprehension,

o Conductive Aphasia: poor repetition, but the patient had fluent

o Global Aphasia: Nonfluent aphasia with impaired comprehension =

o Nominal aphasia: patient is unable to name objects

- Dyslexia: patient can not read correctly

- Dysgraphia: patient can not write correctly

- Dyscalculia: patient will not be able to serially subtract 7 from 100

Cannot be done in confused or dysphasic patients

- Immediate memory: ask the patient to repeat the sequence of 5 to 7

Reasoning and problem solving

- Two step calculation

Cranial Nerve examination

Nystagmus: Slow drift to one direction and followed by fast “corrective”

Trigeminal nerve (V)

Test the three divisions and compare both sides

Afferent: Trigeminal nerve.

Facial nerve (VII)

Ask the patient to:

Auditory nerve (VIII)

Glossopharyngeal nerve (IX), Vagus nerve (X)

- Note the patient’s voice:

Accessory nerve (XI)

- Sternomastoid: ask the patient to rotate head against resistance. Compare

Hypoglossal nerve (XII)

Different forms of gait occurs with different pathologies as in the table

Hemiplegic Gait (Circumduction Gait) Stroke

Sensory ataxia (+ve Rombergism) Peripheral neuropathy