Title Page

General and anatomical features of the nervous system 1

Cerebrovascular Disease
Blood supply of the brain 11
Stroke and hemiplegia 15
Subarachnoid Hemorrhage ( SAH ) 35
Seizures and epilepsy 41
The cerebellum and ataxia 50
Extrapyramidal system 57
Chorea 65
Paraplegia 75
Myopathies 88
Myasthenia 97
Motor Neuron Disease 103
Peripheral neuropathy 106
Demyelinating diseases 124
Headache 131
Degenerative spinal disease 149
Peripheral nerve injuries 160
Inability to walk 183
Floppy infant 185
Microcephaly 188
Cranio Synostosis 189
Cerebral Palsy “ Little Disease ” 190
Myelomeningiocele 193
Hydrocephalus 194
Aneurysms 199
Brain Arterio-Venous Malformations ( AVMs ) 202
Meningitis 204
Encephalitis 210
brain Abscess 214
Tetanus 219
Brain Tumors 224
Mental Health and Substance Abuse 232
Substance Use Disorders 241
Schizophrenia 273
Mood disorders 279
Anxiety disorders 287
Obsessive Compulsive Disorder (OCD) 293
Post traumatic stress disorder (PTSD) 297
Psychiatric disorders of old age 299
 Chapter 1: Neurology
General and anatomical features of the nervous system 1

Cerebrovascular Disease
➢ Blood supply of the brain 11
➢ Stroke and hemiplegia 15

Subarachnoid Hemorrhage ( SAH ) 35

Seizures and epilepsy 41

The cerebellum and ataxia 50

Extrapyramidal system 57

Chorea 65

Paraplegia 75

Myopathies 88
➢ Duchenne & Becker 90
➢ Polymyositis ( PM ) 93
➢ Dermatomyositis (DeM) 94
➢ Myotonias 95

Myasthenia 97

Motor Neuron Disease 103

Peripheral neuropathy 106

➢ Diabetic Neuropathy 110
➢ Refsum's Disease 112
➢ Charcot-Marie-Tooth Disease 113
➢ Guillain-Barre Syndrome (GBS) 114
➢ Diphtheritic Neuropathy 116
➢ Leprotic Neuropathy 117
➢ Deficiency Diseases 118

Demyelinating diseases 124

Headache 131
 Chapter 2: Pediatrics
Febrile Convulsions 43

Inability to walk 183

Floppy infant 185

Microcephaly 188

Cranio Synostosis 189

Cerebral Palsy “ Little Disease ” 190

Chapter 3: Neurosurgery
Degenerative spinal disease 149
Peripheral nerve injuries [Plastic S.] 160
Myelomeningiocele 193
Hydrocephalus 194
Aneurysms and AVM 199
Brain Arterio-Venous Malformations ( AVMs ) 202
Brain Abscess 214
Brain Tumors 224

Chapter 4: Tropical
Meningitis 204
Encephalitis 210
Brain Abscess 214
Tetanus 219

Chapter 4: Mental Health and Substance Abuse [ Community ] 232

 Chapter 5: Psychiatry & Toxicology
Substance Use Disorders 241

Alcohol Related Disorders 243

Alcohol use disorders 251

Opioid Related Disorders 254

chronic opioid abuse 258

Sedatives, hypnotics or anxiolytic related disorders 260

Symptoms with chronic abuse 267

Stimulant related disorders 268

Symptoms with chronic abuse 271

Cannabis related disorders 272

Schizophrenia 273

Mood disorders 279

Anxiety disorders 287

Obsessive Compulsive Disorder (OCD) 293

Post traumatic stress disorder (PTSD) 297

Psychiatric disorders of old age [ Dementia ] 299

 GENERAL AND ANATOMICAL FEATURES
OF THE NERVOUS SYSTEM

is the science and techniques of studying the site, causes and nature
Neurology:
of the nervous system diseases with their diagnosis and therapy.

❖ Neuro-anatomy: is the study of the form of the nervous system.

❖ Neuro-physiology: is the study of the function of the nervous system.

❖ Neuro-pathology: is the study of the nature and extent of the lesions.

❖ Neuro-radiology: is the study of the various modes of investigation used in nervous sys.

❖ Neuro-pediatric: is the study of the diseases of the nervous system in pediatrics.

❖ Neuro-surgery: is art of surgical problems in nervous system diseases.

❖ Neuro-ophthalmology: is the study of the visual system and ocular nerves disorders in
relation to the nervous system.

Anatomical features of the nervous system

 There are two main divisions of the nervous system:-

(1) Central Nervous System ( CNS ):
- Brain & Spinal Cord … both are enclosed & protected in:
1) bone ( skull and vertebral column )
2) protective coverings ( meninges )
3) fluid filled spaces ( CSF )

(2) Peripheral nervous system:

- Cranial nerves and their nuclei
- Roots → Spinal nerves...till the muscles

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 The Central Nervous System (CNS)

A. The Brain

- is nearly about 2% of the total body weight ( 1.5 - 2 kg in adult)

- contains billions of neurons ( nerve cells ).
- Nerve cells with common form, function and connections:
➢ Within the CNS are grouped together to form neuclei
➢ Outside the CNS are grouped together to form ganglia

❖ Brain is formed of: (A) Cerebrum (B) Brainstem (C) Cerebellum

(A) The cerebrum:

- Is composed of two cerebral hemispheres with…

➢ outer grey matter ( cerebral cortex ) composed of nerve cells.

➢ Inner sub-cortical white matter composed of nerve fibers.
- The two cerebral hemispheres are connected to each other by the corpus callosum.

- The interconnections between various parts of the brain are through horizontal
connections called commissures, and through bundles or tracts

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(A) The Cerebral cortex:
- The cortex is divided functionally & anatomically into lobes and areas of specific function,
with thickness of 2 - 4.5 cm.
1) The Frontal lobe:
- Concerned mainly with control of movements.
- Lies anterior to the central sulcus …. contains:
1) Motor area ( 4 ):
 In the floor of the central sulcus.
 it is concerned with initiation of the voluntary motor activity of the opposite half
of the body.

2) Pre-motor area ( 6 ):
 In the anterior part of the pre-central gyrus
 it shares the function of area 4

3) Motor speech center ( Broca’s area 44 ):

 In the middle part of the inferior frontal gyrus of the dominant hemisphere.

4) Writing center ( Exner’s area 45 ):

 Lies in the posterior part of the middle frontal gyrus.

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 5) Area 8 of voluntary conjugate eye movement:
 Lies in the posterior part of the middle frontal gyrus
 it causes conjugate eye movements to the opposite side of stimulation.

6) Pre-frontal area:
 Occupies the anterior pole,
 it is concerned with higher mental functions….
1) memory 2) orientation 3) thinking
4) intelligence 5) personality

2) The Parietal lobe:

- Concerned mainly with sensation.

- Lies behind the central sulcus

- Areas of particular importance include:

1) Cortical sensory areas ( 1 , 2 , 3 ):

 In the post- central gyrus
 concerned with perception of cortical sensations from the opposite half of
the body
2) Visual psychic area ( 39 ) of speech:
 In the dominant hemisphere
 concerned with recognition of the written speech

3) The temporal lobe:

- Lies below the lateral sulcus ( fissure of sylvius ), includes the following areas.

1) Auditory sensory area ( 41 , 42 ):

 Lies in the superior temporal gyrus,
 concerned with hearing.
2) Auditory psychic area ( 22 ):
 lies posterior to the auditory sensory area in the dominant hemisphere
 it is concerned with recognition of sounds.
3) Uncus:
 Lies in the medial temporal lobe,
 concerned with smell and memory.

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 4) The occipital lobe:
- concerned mainly with vision

- Lies behind the parito-occipital sulcus …. contains:

1) Visual sensory area ( 17 ): concerned with reception of vision.

2) Visual psychic area ( 18, 19 ): Concerned with recognition of what is seen by area 17

- In the depth of each cerebral hemisphere, there are certain principal grey nuclei:

a) Thalamus & hypothalamus

b) Basal ganglia:
1. caudate nucleus 2. lentiform nucleus 3. globus
4. pallidus 5. putamen

(B) The brain stem: Consists of three parts from above – below…
1) Mid brain 2) Pons 3) Medulla oblongata.

- Is largely made up of ascending & descending & decussating tracts which join the
different parts of the brain and spinal cord, together with the brain stem

- the brain stem relates to the cerebellum which lies behind it through 3 cerebellar
peduncles.

❖ The brain stem in addition contains important structures such as:

1) The cranial nerve nuclei: which are…
• Nuclei of cranial nerves (3) and (4) in the mid brain.

• Nuclei of cranial nerves (5), (6), (7) and (8) in the pons.

• Nuclei of cranial nerves (9), (10), (11) and (12) in the medulla

2) The Reticular formation: which is related to…

➢ sleep ➢ consciousness
➢ behavior ➢ memory

3) Respiratory, Cardiac and Vomiting centers.

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(C) The cerebellum:
❖ Anatomically:
- consists of 2 cerebellar hemispheres & 3 cerebellar peduncles that connect it with the
brain stem

❖ Functionally: it can be divided into - 3 - divisions:

1) Archi-cerebellum → concerned with equilibrium

2) Paleo-cerebellum → concerned with muscle tone & automatic movements

3) Neo-cerebellum → concerned with coordination of fine movements

B. The spinal cord ( myelon & medulla spinalis )

- Is an elongated structure, about 42 - 45 cm long in adults

- Its upper end continuous with the brain stem at the foramen magnum and extends to
the lower border of the 1st lumber vertebra.

- The rest of the spinal canal is filled with filum terminal " extension of pia matter ”.

- The lower tapering border of the spinal cord is termed conus medullaris.

- The cord is divided into 31 segments:

➢ (8) Cervical ➢ (12) thoracic ➢ (5) lumbar ➢ (5) sacral ➢ (1) coccygeal

- There are two enlargements; cervical and lumbar enlargements with

the brachial plexus & lumbar plexus originate from those enlargements in order

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- In contrast to the brain, the cord consists of inner H shaped grey matter surrounded by
the white matter…
1) The grey matter consists of:
a) 2 posterior horns " sensory "
b) 2 anterior horns " motor "
c) intermedio-lateral horns in the thoracic & sacral regions
 for sympathetic & parasympathetic efferents

2) The white matter: contains many ascending and descending tracts

The peripheral nervous system:

 Consisting of…
1) The cranial nerves with their nuclei
2) Anterior horn cells (AHC)
3) Spinal nerves peripheral nerves
4) Neuromuscular junctions and the muscles

- From the cerebral cortex to the spinal cord this is called upper motor neurons
- From the AHC till the muscles this is called lower motor neurons
 both has characteristic clinical features

Organizations of movements in the motor system

- For normal voluntary motor activity, the following parts of the nervous system
must be normal and cooperate::
1) The motor areas, corticospinal tract "pyramidal tract” ( UMN )
2) The lower motor neurons ( LMN ).
3) The basal ganglia.
4) The cerebellum.

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 The components of the motor system

1. The pyramidal tract:

- Constitutes the descending pathway which arise from the giant cortical Betz cells of the
motor and pre-motor areas.

- There is a wide presentation of the body in the cortex and it is presented upside down.

- The nerve fibers descend in the cerebral hemisphere in a collecting manner.

- The pyramidal tract in human contains about 1 million fibers, 94% of which are
myelinated
- The descending fibers comes together in the corona radiate → then to be collected
more in the Internal capsule ( lies deep in the cerebral hemisphere ) where it occupies:
1) the post 1/3 of the anterior limb
2) the genu
3) the anterior 2/3 of the posterior limb

- From the internal capsule the tract descends through the middle 3/5 of the cerebral
peduncle to enter the mid brain
 Then to the pons where it is broken into bundles by the transverse pontine fibers
 Then to the medulla where it occupies an anterior prominence ( pyramid )

- Throughout the brain stem the pyramidal tract gives off the corticobulbar tract which
supply the nuclei of the motor cranial nerves of the opposite side

- In the lower part of the medulla > 80% of the pyramidal tract decussates ( cross to the
other side ) to form the crossed tract which descends in the lateral column of the
spinalcord on the opposite side.

- the remaining uncrossed fibers descend on the same side in the anterior column
forming the direct pyramidal tract.

- All the cranial nerve nuclei receive bilateral cortical supply except….
1) the lower half of the facial
2) the hypoglossal nuclei
 which receive only contralateral cortical supply

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2. The basal ganglia and the cerebellum:
- Information for normal motor activities before passing to the spinal cord and the final
organized station " the lower motor neurons " must pass at first through the basal
ganglia and the cerebellum through the different connections between :
( the cerebral cortex / brain stem / spinal cord )

❖ The basal ganglia: has the following influence on the motor system..
1) Regulation of posture.
2) Plays a vital role in initiating movements… Lesions → akinesia or bradykinesia
3) Gives off smooth coordinating voluntary motor activity.
4) Regulation of muscle tone and voluntary movements … Lesions → rigidity & tremors

❖ The cerebellum: shares in the organization of the motor system activity through:
1) Regulation of postural reflexes and equilibrium… lesions → unsteadiness
2) Regulation of muscle tone… lesions → hypotonia
3) Regulation & smooth coordination of limb movements… lesions → ataxic movements

3. The lower motor neurons:

- Forming the final process in organizing motor activity,

- it constitutes the following:

1) Nuclei of motor cranial nerves.

2) Anterior horn cells of the spinal cord →

giving off the anterior roots which form with the afferent posterior roots →

the spinal nerves → which will form the peripheral nerves →

neuro-muscular junction → into the muscles

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 IN CONCLUSION

- In response to the afferent stimuli or desire to do voluntary activity,

- the stimuli will travel through the afferents up to the cortex, passing through
the spinal cord → then, from the cortical motor area → efferent stimuli will descend →
corona radiata → Internal capsule → spinal cord → lower motor neurons to initiate the
desired movement, through activation of specific AHC and the motor units they supply

- At the same time, information about the required movement reach the basal ganglia and
the cerebellum to regulate, coordinate, smooth, counteract any undesired movements

- simultaneously, as the required muscles "agonist" are being stimulated to contract…

1) the synergists " helper " contract to assist
2) the fixators contract to fix
3) the antagonists → relax.

- Once the required movement have begun, it is then continuously modified and
maintained if needed through continuous afferent sensory impulses arriving the motor
system components from:
1) the deep sensory receptors,
2) eyes
3) labyrinths

- Therefore, lesions in any of the above parts involved in initiating and controlling motor
activity will result in disorganized, abnormal movements.

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 CEREBRO-VASCULAR DISEASE

Blood supply of the brain

- The brain is about 2% of the total body weight,

- receives 15% of the cardiac output and 25% of the total inspired air 02.

- The cerebral blood flow (C.B.F) is about…

➢ 50-60 ml blood /100gm brain/minute in the vital grey matter
➢ about 40ml blood /100g brain /minute in the white matter.
- If the cerebral blood flow is below ( < 10ml /100gm/minute ) infarction will occur and
even if flow is restored, the function does not recur

- The rich blood supply is carried to the brain through…

a) 2 internal carotid arteries
b) 2 vertebral arteries
 which anastomose at the base of the brain forming the circle of Willis.

I. The carotid system ( the anterior circulation )

- Each internal carotid artery ( I.C.A ) starts as a branch of the common carotid artery at
the level of the upper border of the thyroid cartilage, enters the base of the skull through
the carotid canal → it then runs through the cavernous sinus where it gives the small
branches →
- Finally, the I.C.A terminates by dividing into its 2 terminal branches:

A. The anterior cerebral artery ( ACA ):

- pass on the medial surface of the cerebral hemisphere and anastomose with its
counter part of the opposite side via the anterior communicating artery.
- It supplies:
1) Anterior & medial parts of the cerebral hemisphere.
2) Anterior basal ganglia & the internal capsule ( anterior limb - genu )
3) Parts of ( the optic nerve - optic chiasma - hypothalamus )

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B. The middle cerebral artery ( MCA ):
- Runs on the lateral surface of the cerebral hemisphere to supply:

1) Most of the lateral parts of the cerebral hemisphere

2) Lenticulostriate arteries and arterioles to supply:
➢ the basal ganglia
➢ the ant. 2/3 of the post, limb of the internal capsule

The external carotid artery

- which is the other branch of the common carotid artery, supplies:
1. { the jaw - face - neck - meninges } mainly through the branch of the middle
meningeal artery
2. { the scalp } through the superficial temporal, occipital, and the posterior
auricular arteries
 The external carotid artery does not share in the circle of Willis.

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 II. The vertebra-basilar system ( the posterior circulation )

- Formed of 2 vertebral arteries, each arise from the 1st part of the subclavian artery
and ascends through the transverse foramina of the first six cervical vertebrae giving off
small muscular branches →
- then enters the skull through the foreman magnum, unites with the opposite one at
the ponto-medullary junction to form the basilar artery which ascends upwards to
the ponto-midbrain junction where it divides into its 2 terminal posterior cerebral
arteries.

❖ Branches of the vertebral artery:

1) To the meninges

2) Anterior and posterior spinal arteries to

the spinal cord.
3) Posterior inferior cerebellar artery to
the cerebellum.
4) Small penetrating arteries to the medulla.

❖ Branches of the basilar artery:

1) The anterior inferior cerebellar artery.

2) The superior cerebellar artery.

3) The internal auditory artery.

4) Small penetrating branches to

the brain stem.

❖ The Posterior cerebral artery:

- Encircles the mid brain supplies….

1) the Inferior part of temporal lobe.

2) Occipital lobe.
3) Midbrain - thalamus - hypothalamus - geniculate bodies.
4) Posterior 3rd of the posterior limb of the internal capsule

 Each posterior cerebral artery communicates with the ipsilateral middle cerebral
artery through the posterior communicating artery.

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 Regulation of the cerebral blood flow (CBF)

1) Arterial C02 tension:

 arise of Pa CO2 of 1 mmHg → causes an immediate increase in CBF of 5%.

2) Arterial 02 tension: its effect is less than that of CO2

3) Blood viscosity ( hematocrit ): CBF is inversely related to the whole blood viscosity

4) Arterial blood pressure:

 CBF remains constant when the mean systemic blood pressure is between
60 -160mmhg which is known as auto regulation.
 Decrease systemic arterial blood pressure → vasodilatation → increase CBF
→ until exhaustion occurs → oligemia and ischemia.
 Increase systemic blood pressure → vasoconstriction → decrease CBF
→ until exhaustion occurs → hyperemia and ischemia.

❖ Auto regulation is impaired in:

1) Metabolic impairment. 2) Organ failure 3) Elderly MODE
4) Previously Damaged brain ( e.g., old stroke, trauma ... )

In chronic hypertensive patients, the autoregulation range is shifted upwards

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 STROKE & HEMIPLEGIA

❖ Stroke:
- Is a rapidly developing clinical symptoms and/or signs of focal or global loss of cerebral
function, lasting more than > 24 hours or leading to death, with no apparent cause other
than that of vascular origin.

- It's one of the four leading causes of death in most countries and the leading cause of
severe neurologic disability in adults.

- They are either ischemic ( ∼ 85% ) or hemorrhagic ( ∼ 15% ).

 Cerebrovascular diseases include:

1) Cerebral infarction ( thrombosis & embolism )
2) Hypertensive encephalopathy.
3) Transient ischemic attacks ( TIA ) .
4) Intracranial hemorrhage ( Epidural - Subdural - Subarachnoid - intracerebral
and intraventricular )

❖ Transient ischemic attacks ( TIA ):

- Transient focal neurological deficits lasting for less than < 24 hours, usually minutes of
vascular ischemic origin with complete recovery.

Risk factors for stroke

1) Age:
- is the strongest and inevitable risk factors of stroke.
- stroke in people aged 75 - 84 years is 25 times the risk in people aged 45 - 54 years.

2) Sex:
- there is small male excess of strokes mainly in middle age most probably due to
prophylactic role of endogenous sex hormone in females ( estrogen ).

3) History of TIA or stroke

4) Family history of stroke

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5) Hypertension:
- either elevated diastolic or systolic blood pressure is associated with increased risk,

- with each 7,5 mm Hg increase in Diastolic blood pressure stroke risk Doubles.

N.B: HTN also in aged atheromatous cerebral vessels causes strokes ( infarction )
6) Hyper-coagulability:
- with increase plasma fibrinogen, increase hematocrit, risk of stroke is increased
( polycythemia ).

7) DM: doubles the risk of stroke compared with non-diabetics.

8) Dyslipidemia:
- with high levels of LDL and decreasing HDL level is a high- risk factor for stroke and
coronary heart diseases.
- A reduction of plasma cholesterol by 10% reduces risk of coronary by 20%.

9) Drug induced stroke:

1) Hypotensive drugs.
2) Cytotoxic drugs → thromboembolic strokes.
3) Aspirin & anticoagulants
4) Thrombolytic therapy.

10) Dietary habits:

➢ Diet rich in…
• fatty fish • folic acid • vitamin E, C
• fresh fruits & vegetables • selenium
➢ with moderate salt intake
➢ & high k

 has a protective value.

11) Alcohol consumption:

a) increases the blood pressure & blood lipids
b) usually associated with ( AF - cardiomyopathy )
 consequently increase the risk of stroke.

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12) Coffee: Consumption of boiled unfiltrated coffee has a small hyper lipidemic effect.

13) Cardiac diseases:

- e.g. ( CAD - HF - A.F - valvular diseases - arrhythmias ) all are important risk factors
for embolic infarction.

14) Cigarette smoking:

- an important risk factor for stroke either infarction or hemorrhage ( doubles stroke ).

- Recently reported to be one of the major 5 risk factors of stroke

15) Contraceptive pills:

- with high doses of estrogen >50 ug → triple the risk of stroke

- while lower doses of estrogen lower the risk, therefore post-menopausal estrogen
replacement may have some protective effect.

16) Chronic stress.

17) Body built: Obesity mainly truncal obesity… { BMI → risk of stroke }

18) Physical inactivity 19) Lower social class

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 HEMIPLEGIA

Causes of hemiplegia

1) Vascular ( STROKE ) : either ischemic or hemorrhagic

2) CNS infections: brain abscess - encephalitis.
3) Brain tumors: meningioma - glioma, ….etc.
4) Demyelinating: DS - DEM
5) Trauma: cerebral laceration - subdural hematoma.
6) Congenital cerebral palsy.
7) Hysterical: the patient suffers from paralysis although there is no organic pyramidal
tract lesion.

Clinical presentation & localization of a case of hemiplegia:

 varies much according to:

1) The site of the lesions in the nervous system.
2) Etiology of hemiplegia.

❖ General clinical features:

1. Onset:
1) usually acute in hemorrhage
2) may be subacute in thrombosis
3) sudden in embolic
4) gradual in neoplasm
5) intermittent in D.S

2. Course: may be…

➢ Regressive in: inflammatory causes - vascular - traumatic causes
➢ Progressive in: neoplasm.

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3. Weakness:
- is usually affecting one half of the body UL, LL in equal degree or one may be affected
more than the other
- weakness affects group of muscles, affecting fine movements more
- Distal muscles are more affected
- Pro-gravity muscles are more affected than anti-gravity i.e…
a) In UL → Extensors are weaker b) In LL → Flexors are weaker

4. Muscles tone:
a- In acute lesions:
• there is a shock stage lasting for 2 - 6 weeks,
• during which there is a complete loss of tone of the paralyzed side,
• after this stage tone gradually returns and spasticity appears
b- In gradual lesions:
• spasticity develops from the start
• Adductors are more affected than abductors
• Anti-gravity muscles are more affected than pro-gravity muscles i.e….
a) UL → Flexors are more spastic b) LL → Extensors are more spastic

5. Reflexes:
1) Deep tendon reflexes in the affected limbs are exaggerated
2) Pathological reflexes & clonus may be elicited.
3) Superficial reflexes:
➢ +ve babinski sign
➢ lost abdominal & cremasteric on the affected side.

In the shock stage: deep reflexes are lost or diminished

6. Gait: is usually circumduction.

7. Other features of sensory impairment & cranial nerves affection dependent on

site of the lesions as shown later in discussion of localization

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 Clinical approach in localization of the site of the lesion in hemiplegia:

❖ Hemiplegia occurs in lesions affecting the pyramidal tract along its course from:
1) Cerebral cortex ( cortical lesions )
2) Sub cortical lesions
3) Capsular
4) Brain stem ( mid brain - pons - medulla ).
5) Spinal cord up to segment 5

1) Cortical lesions:
- Usually hemiplegia is not complete, monoplegia is more encountered due to the wide
origin of pyramidal tract and weakness is contralateral

- Cloudiness of consciousness: is common.

- Contra-lateral cortical sensory loss: in involvement of the parietal lobe.

- Convulsions: which may be focal or secondary generalized, in cases of irritative

extensive lesions.

- Higher mental functions disorders: e.g. ( aphasia - agraphia - agnosia )

in lesions affected specific lobes, centers, or sites.

2) Subcortical lesions: As in cortical but weakness is more extensive.

3) Capsular: the commonest

- Hemiplegia is complete
- Hemi-hypothesia on the paralyzed side ( common ).
- UMN facial and hypoglossal on the same side of paralysis ( common ).
- No convulsions & aphasia or coma.

4) Brain stem: is termed crossed hemiplegia, characterized by:

1) hemiplegia on the opposite of the lesion
2) with LMN cranial nerves affection on the same side of the lesions ( opposite to the
hemiplegia ).

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 a) Mid brain syndromes:
1. Weber's syndrome:
 Ipsilateral 3rd cranial nerve lesion  Crossed hemiplegia ( contra lateral )
2. Benedict’s syndrome:
 as above + hemiataxia on the opposite site of the lesion ( red nucleus affection )

b) Pons syndromes:
1. Millard Gubler’s syndrome:
 Ipsilateral 6th, 7th cranial nerves lesion  Crossed hemiplegia
2. Foville’s syndrome:
 Ipsilateral loss of conjugate eye movement  Crossed hemiplegia

c) Medullary syndromes:
1. Wallenberg syndrome:
 Ipsilateral:
1) 9th , 10th , 11th cranial nerves 2) Ataxia
3) Decrease sensation over the face 4) Horner's syndrome
 Contra lateral hemi-anesthesia

2. Avillis syndrome:
 Ipsilateral 9th , 10th Cr. N paralysis.  Crossed hemiplegia

3. Jackson’s syndrome:
 Ipsilateral 11th , 12th Cr. N. +  Crossed hemiplegia

5) Spinal cord lesions ( Browen Sequard's Syndrome ):

- In hemi lesion of the spinal cord in upper cervical segments, hemiplegia may occur
with the following features:
a. At the level of the lesions:
1) Ipsilateral LMN weakness of muscles supplied by the affected segments.
2) Loss of reflexes mediated by the interrupted segments.
3) Loss of sensation ( radicular ) in the area supplied by the diseased segments.

b. Below the level of the lesion:

4) Ipsilateral hemiplegia 2) Ipsilateral deep sensory loss
3) Contralateral superficial sensory loss.
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 Differential diagnosis of stroke

- The diagnosis of stroke versus non-stroke is straight forward if there is a history of

acute or sudden onset of focal neurologic deficits of vascular origin,

- if the history is not clear C.T will solve the problem, but clinically the followings must be
differentiated:

1) Brain tumors:
• history of [ headache - papilledema - seizures - blurring of vision ]
• with gradual onset & progressive course

2) Chronic subdural hematoma:

• history of: head injury ( weeks up to years before )
• more [ drowsiness - confusion - headache ] than the focal deficits.

3) Encephalitis:
• acute or subacute onset of fever • cloudiness of consciousness
• convulsions • signs of meningeal irritation
• higher mental function disorders.

4) Brain abscess:
• history of [ fever - headache ]
• with signs and symptoms of [ increased ICT - focal deficits ]
• with source of infections e.g. [ mastoiditis - OM - congenital heart diseases ]

6) Todd’s paralysis: history of epileptic seizures of focal onset.

7) Hysterical hemiplegia: usually occurs in young age with no + ve data on examination

22
 1. ISCHEMIC STROKE

Definition

- Rapidly developing focal disturbance of cerebral function due to insufficient cerebral

blood flow ( hypoperfusion ), which results in ischemia and neuronal injury, lasting for
more than > 2 hours or leading to death.

Causes

1) Embolic strokes ( 20% ):

- It's due to embolism in the cerebral arteries coming from other parts of the arterial
system.
- Most commonly affect the middle cerebral artery ( MCA )

a) Cardiac emboli ( 75% of cardiac emboli go to the brain ).

1. AF in MS, 2. Atrial or ventricular thrombi,
3. Rheumatic heart disease, 4. Ventricular aneurysms.

b) Atherosclerotic emboli: Internal carotid artery and Aortic arch ( less common ).

c) Infectious emboli: bacterial endocarditis.

d) Paradoxical embolism: in patients with right-to-left cardiac shunt: e.g.

1. persistent foramen oval 2. atrial septal defect

2) Thrombotic strokes ( ∼ 40% ):

- Caused by atherosclerotic obstruction of large cervical and cerebral arteries, with
ischemia in all or part of the territory of the occluded artery.
a) Large vessel atherosclerosis ( ∼ 20% )
- Thrombus formation most commonly occurs at branch points in arteries: e.g.,
1. internal carotid artery bifurcation
2. where the MCA branches from the circle of Willis

b) Small vessel occlusion ( lacunar infarct ) ( ∼ 20% ).

23
3) Global cerebral ischemia:
a) Systemic hypoperfusion:
- shock or bilateral large artery atherosclerosis ( e.g., of carotid arteries ) → decreased
effective oxygen delivery to the whole brain.

b) Hypoglycemia:
- repeated episodes of hypoglycemia ( e.g., due to insulinoma ) increase the risk of
cerebral ischemia.

c) Severe and/or chronic hypoxia:

- hypoxemia ( e.g., due to respiratory arrest ) → global tissue hypoxia in the brain.

4) Other causes:
a) Hypercoagulable states:
1. Inherited thrombophilia ( e.g., factor V Leiden mutation - protein C deficiency ),
2. Polycythemia,
3. Hormonal contraceptive use,
4. Hormone replacement therapy,
5. Sickle cell disease.

b) Vasculitis: e.g., giant cell arteritis

c) Arterial dissection: e.g., due to trauma or fibromuscular dysplasia

Risk factors for ischemic stroke

1) Old Age ( > 65 y ) [ 75% of all strokes ].

2) Race ( African > Hispanics > Caucasians )

3) Sex ( Male more ).

4) Family history of ischemic stroke.

5) Previous stroke, Transient ischemic attacks or myocardial infarction.

6) AF 7) Hypertension 8) Diabetes mellitus

9) Dyslipidemia 10) Smoking 11) Obesity

12) physical inactivity 13) Cardiovascular disease 14) Coronary artery disease.

24
 Pathophysiology of ischemic stroke

- Ischemic stroke is caused by focal cerebral ischemia: a localized reduction in blood flow
sufficient to disrupt neuronal metabolism and function.

- If ischemia is not reversed within a critical period, irreversible cellular injury ensues,
resulting in cerebral infarction.

- An area called a PENUMBRA may result, denotes the part of an acute ischemic stroke
that is at risk of progressing to infarction but is still salvageable if re-perfused. It is usually
located around an infarct core ( which represents the tissue which has already infarcted
or is going to infarct regardless of reperfusion ).

- The primary aim of current acute stroke intervention is to prevent the penumbra from
proceeding to established infarct.

Clinical Picture

A. General:
- Typically, new symptoms in ischemic stroke develop over seconds to minutes, or they
may be present on waking from sleep.

1) Nausea & vomiting: may occur, particularly with brainstem & cerebellum lesions.

2) Decreased level of consciousness: is unusual in the first several hours after

ischemic stroke, unless the brainstem reticular activating system is affected.

3) Hypertension: is present acutely in more than > 70% but often returns to baseline
spontaneously over the next several days.

4) Neurologic deficit: varies according to cerebral territory affected.

B. Specific picture: [ see hemiplegia ].

1) Thrombotic Strokes ( large artery thrombosis ): 40% of all strokes
- Usually occurs during sleep ( patient often awakens unaware of deficits ).
- May have “ stuttering “ intermittent progression of neurologic deficits or be slowly
progressive ( over 24 - 48 h. )
- Profound loss of consciousness is rare except when area of infarction is large or when
brainstem is involved.

25
 - Emboli from incompletely thrombosed artery may precipitate an abrupt deficit.
May have embolism from extracranial arteries affected by stenosis or ulcer.

2) Embolic Strokes: 20% of all strokes

- Usually occurs during waking hours.
- Immediate onset of neurologic deficits.
- Seizures may occur at onset of stroke.

Investigations

A. Imaging studies:
1) Non contrast CT Brain: the most used
- Immediately to exclude mimics:
[ Intracerebral hemorrhage (ICH) or Subarachnoid Hemorrhage (SAH) or masses ]
- Infarction not seen immediately ( unless if there is a mass effect )
- Follow-up CT: done after 48 h. to confirm the diagnosis of ischemic stroke.
- Infarction in CT: locally decreased density ( hypodense ) = darker than normal
i.e BLACK

2) MRI Brain:
- infarction can be seen immediately.
- More sensitive than CT in detecting acute ischemic infarcts

- Diffusion-weighted imaging ( DWI ) – MR: is the most sensitive

3) Carotid Ultrasound: Screening test for carotid stenosis.

4) ECG & Echocardiography: for evaluation of cardiac causes such as:

1. Dilated cardiomyopathy
2. Apical thrombus
3. Valvular thrombus
4. Endocarditis
5. Patent foramen oval
6. Aortic arch atherosclerosis

5) Laboratory markers of Thrombophilia.

26
B. Laboratory studies:
1) CBC: may reveal a cause for the stroke e.g.
1. polycythemia 2. leukemia 3. thrombocytosis 4. thrombocytopenia

2) Basic laboratory evaluation of [ electrolytes - glucose - liver & kidney

function tests ]:
1. may reveal a stroke mimic ( e.g. hypoglycemia or hyponatremia )
2. provide evidence of concurrent illness (e.g. diabetes or renal insufficiency).

3) Cardiac biomarkers

4) Fasting lipid profile

5) Uric acid serum level

6) Coagulation parameters i.e. ( INR ) & ( PT ) & ( aPTT ):

❖ Thrombophilia workup: Indicated for unexplained stroke in young patients ( < 50 y )
who has a history of thrombosis or clinical suspicion of hypercoagulable state e.g.
1. Protein C & Protein S
2. Antiphospholipid antibodies

Treatment

❖ General principles:
1) Stabilize the patient's general condition.

2) Give therapy directed at specific aspects of stroke pathogenesis ( e.g., recanalization

of vessel occlusion or a prevention of mechanisms leading to neuronal death ).

3) Treat complications such as:

1. 2ry hemorrhage 2. space occupying edema 3. seizures
4. infection 5. decubital ulcers 6. DVT
7. pulmonary embolism 8. aspiration

4) Initiate early 2ry prevention measures to reduce incidence of stroke recurrence.

5) Begin rehabilitation measures.

27
A. Acute Ischemic Stroke Treatment:
1. Thrombolysis:
- with recombinant tissue plasminogen activator ( rt-PA ): Alteplase .. is the only
FDA-approved medication for acute ischemic stroke.
- It must be given within 3 - 4.5 h. ( golden time window ) from the onset of symptoms.

❖ Inclusion criteria:
1) Symptoms suggestive of ischemic stroke that believed to be disabling.
2) Able to initiate treatment within 4.5 h of Time Last Known Well.
3) Age 18 y or older.

❖ Contraindications:
1) Intracranial hemorrhage (e.g., ICH or SAH) history or presence on imaging.
2) Brain CT demonstrates large infarction.
3) Elevated Blood pressure greater than > 185 / 110 mm Hg.
4) Recent ( within 3 months ) severe head trauma or neurosurgical operation.
5) INR > 1.7 - Thrombocytopenia - recent use of heparin or direct oral anticoagulants
6) Intracranial neoplasm or aneurysm.
7) Active internal bleeding,

❖ Complications:
1) Bleeding.
2) Angioedema.
3) Intracranial & extracranial hemorrhage.

2. Intra-Arterial Mechanical Thrombectomy:

- Thrombectomy ( i.e. retrieval of the occluding thrombus via a catheter) devices can
be useful in achieving recanalization alone or in combination with pharmacological
fibrinolysis in carefully selected patients.
❖ Indications: large artery occlusion in anterior cerebral circulation.

NO benefit of immediate anticoagulant therapy in acute ischemic stroke

28
B. Secondary Prevention of Ischemic Stroke ( prevent recurrence ):
1. Antiplatelet agents: ( for thrombotic stroke )

 If there is no active bleeding or other contraindication.

1) Aspirin: 75 - 325 mg/day. Significant reduction of recurrent stroke or
2) Clopidogrel ( Plavix® ): 300 mg load, then 75 mg/day.

2. Anticoagulants: ( only with cardioembolic stroke ) e.g.. AF

1) Warfarin ( Marevan ): Indicated in….

1. hypercoagulable states
2. cardiac sources like { AF or intracardiac thrombi }
2) Dabigatran ( Pradaxa ):
- Indicated in persistent or paroxysmal nonvalvular AF.
- Better than warfarin.

3) Rivaroxaban ( Xarelto ): factor Xa inhibitor.

- Reduce the risk of stroke & systemic embolism in nonvalvular AF
- Better than warfarin.

4) Apixaban ( Eliquis® ): Same as Rivaroxaban.

3. Risk Factors treatment:

1) Care of Blood Pressure ( BP ):
- Anti-Hypertensive drugs if the BP is above 200/120 mm Hg.

- Avoid sudden marked reduction of BP which decreases cerebral blood flow and
worsens brain ischemia.

2) Statins & cholesterol-lowering agents:

- Shown to lower the risk of atherosclerotic mortality & vascular events including
stroke

3) Smoking cessation
4) DM control
5) a low-fat & low-salt diet
6) weight loss & regular exercise.

29
❖ Other drugs may be used:
1) Piracetam ( Nootropil® ):
- It improves brain metabolism by increasing 02 consumption.
- It also decreases blood viscosity by reducing platelet aggregation.

2) Pentoxifylline ( Trental® ):
- It improves the microcirculation of the brain by…
1. increasing RBCs deformability
2. reducing platelet aggregation.

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30
 2. TRANSIENT ISCHEMIC ATTACK ( TIA )

Definition

- A transient episode of neurological dysfunction caused by focal transient brain or retinal

ischemia, with clinical symptoms typically lasting minutes up to 1 hour ( maximum 24h )
without evidence of acute infarction on brain imaging.

Causes & Investigations: The same causes of ischemic stroke

Treatment

I- Medical:
a. Antiplatelet aggregating drugs: they reduce incidence of strokes by about 50%.
1) Acetyl-salicylic acid ( Aspirin ): 75-300 mg daily.
2) Clopidogrel: 75 mg daily.

B. Anticoagulant drugs as warfarin;

- in hypercoagulable states, cardiac sources like atrial fibrillation & intracardiac thrombi.
( Target INR = 2 - 3 )

C. Other drugs: used with the antiplatelet drugs as piracetam, pentoxifylline or piribedil.

D. Treatment of any risk factor.

II. Surgical:
❖ Carotid endarterectomy or carotid artery stenting:
- is used in: carotid artery stenosis of over 70% to relieve recurrent TIAs and to prevent a
major stroke.
- It is not used in: mild stenosis or if a stroke has already occurred.

Prognosis after TIA

• 5% stroke risk within 2 days.

• 10% stroke in 90 days ( 21% fatal & 64% disabling ).
• 1 in 9 patients will have a stroke within 3 months
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 3. HEMORRHAGIC STROKE

Definition: Intracranial hemorrhage may be:

1) Intra-cerebral hemorrhage ( ICH ): bleeding within the brain parenchyma.

 The commonest artery causing ICH is the lenticulo-striate branch of the MCA.

2) Intra-ventricular hemorrhage ( IVH ): bleeding within the ventricles.

 IVH is very serious as the blood may compress vital centers.

3) Subarachnoid: the bleeding is in the subarachnoid space.

4) Subdural or extradural: the blood often forms a hematoma.

Commonest sites for ICH: 1. Basal ganglia 2. Lobar regions 3.Thalamus

Common causes of ICH

1) Hypertension 2) Anticoagulants
3) Thrombocytopenia 4) Bleeding tendencies ( hemophilia )
5) Thrombolytic drugs 6) Vascular malformations.
7) Trauma. 8) Bleeding into brain tumors and brain infarcts.
9) Cerebral amyloid angiopathy: most likely cause of spontaneous lobar ICH in patients
> 55 years

Pathophysiology of hemorrhagic stroke:

- Blood from an ICH accumulates as a mass that can dissect through and compress
adjacent brain tissues, causing neuronal dysfunction.
- Large hematomas increase ICP.
- If the hemorrhage ruptures into the ventricular system ( IVH ),blood may cause
acute hydrocephalus.
- Cerebellar hematomas can expand to block the 4th ventricle, also causing
acute hydrocephalus.
- { Midbrain or pontine hemorrhage, IVH or acute hydrocephalus } can impair
consciousness leading to coma and death
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 Clinical picture

❖ Hypertensive ICH:
- Linked to chronic Hypertension ( about 35% occur in normotensives ).

- Frequently extends to ventricular subarachnoid space→ IVH.

❖ Symptoms:
1) Sudden onset of headache and/or loss of conscious.
2) Vomiting: at onset in 22-44%.
3) Seizures: 10% of cases ( first few days after onset ).
4) Nuchal rigidity: is common.

Investigations

A. Imaging studies:
1) Noncontract CT Brain: the most used.
- Hyperdense ( white ) lesion seen immediately in ~100% of cases.

- CT is superior to MRI in detecting ICH.

2) MRI Brain

3) Angiography:
- in case of Acute hemorrhage. Angiography should be considered when CT and MRI
do not provide the cause of the hemorrhage.

B. Laboratory studies:
1) CBC 2) Metabolic panel

3) Coagulation studies ( PT - INR - aPTT ) in patients taking anticoagulants.

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 Treatment

1- General care of…

1) Skin 2) respiration 3) nutrition
4) body fluids 5) urinary bladder 6) bowels
7) body temperature

2- Anti-hypertensive drugs: in cases of hypertension.

3- Anti-convulsants: if seizures occurred… It's NOT recommended prophylactically.

4- Replacement of…
1) coagulation factor deficiency or
2) severe thrombocytopenia.
5- Raised ICP: may be treated with…
1) hyperosmolar therapy ( IV mannitol or hypertonic saline )
2) hyperventilation,
3) or neuromuscular paralysis

 Steroids should be avoided.

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 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:
1. axial loading 2. bending 3. shear forces

Site: Cervical disc prolapse more common in { C5-C6 & C6-C7 levels }

149
 Clinical picture

- The prolapse is usually posterolateral causes root compression ( Radiculopathy )

- the prolapse is central it will cause cord compression ( Myelopathy ).
- In case of root and cord compression Radiculomyelopathy occurs.

❖ Symptoms:
1) Neck pain and stiffness.
2) Pain radiating down the arm and hand ( brachialgia )
 exacerbated by neck motion ( extension).
3) Paresthesia, tingling & numbness .. { along the affected dermatome }
4) Motor weakness
5) Sphincteric dysfunction.

❖ Signs:
1. Signs of Radiculopathy: depends on which root is compressed

2. Signs of myelopathy: ( cord compression )

1) Spastic quadriparesis
2) Hyperreflexia below the level of the compression
3) Clumsiness and ataxia of the extremities
4) Gait disturbance
5) Sphincteric disturbance.

150
 Investigations

1) Plain x ray:

a) Loss of lordosis.

b) Narrowing of the disc space.

c) Osteophytes.

2) MRI: the best diagnostic technique.

3) CT scan
4) Myelography: not commonly used

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 due to deficit 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

151
 Cervical Spondylosis

- It is a degenerative change including ( vertebral bodies, neural arches, facet joints,

ligaments & 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

1) Insidious onset.
2) Radiculopathy, myelopathy or radiculomyelopathy
3) Spastic weakness of the lower limbs, with clonus and +ve Babiniski sign.
4) Weak hand grip and clumsiness.
5) Hypoalgesia due to spinothalamic tract affection.

Investigations

1) Plain x-ray cervical spine

2) CT scan

3) MRI: is the most accurate

Management:

❖ Conservative: as in cervical disc prolapse if there is no cord compression

❖ Surgical:
1) Posterior: laminectomy with or without foraminotomy ± Fusion

2) Anterior:

➢ Multilevel discectomy,
➢ removal of osteophytes,
➢ Stabilization by interbody fusion or instrumentation.

152
 Lumbar disc prolapse

Anatomy: Inter vertebral disc consists of:

1) Two cartilaginous end plates.

3) Nucleus pulposus ( softer form of cartilage ).

4) Annulus fibrosus ( concentric layers of fibrous tissue and fibrocartilage ).

Pathophysiology

- Lumbar disc prolapse occurs when the nucleus soft 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% sciatica.
- There is history of falling or lifting heavy weights preceding the onset of symptoms

Site: The majority of LDP occurs at L4-L5 & L5-S1 ( 95% )

153
 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 & has complained of chronic low back pain for some prior to
the onset of acute disorder.
- Herniation occurs either centrally or lateral:
➢ When laterally, it compresses the adjacent nerve root ( Radiculopathy )
➢ When central, it compresses the cauda equine ( Cauda-equine syndrome )

❖ Symptoms:
1) Back pain
2) 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
3) Numbness or tingling occurs in the distribution of the affected root.
4) Motor weakness
5) Bladder symptoms ( urgency, frequency, retention )

❖ Signs:
A. Back signs:
1) Restricted spinal movement.
2) Local tenderness.
3) Scoliosis.
4) Paravertebral muscle spasm.
5) Obliteration of lumbar lordosis.

B. Signs of radiculopathy: depends upon the root compressed

1) Motor weakness
2) Dermatomal sensory changes
3) Reflex changes
C. Clinical tests ( nerve root tension signs ):

154
Level of disc
prolapse
L3 - L4 L4 - L5 L5 - S1

Compressed
L4 root L5 root S1 root
root

Motor Dorsi-flexors of Planter-flexors of

Quadriceps
weakness the foot the foot

1) Posterior part of calf

1) Medial part of calf 1) the Lateral side of calf
2) lateral malleolus
Sensory 2) medial malleolus 2) dorsum of the foot
impairment 3) lateral foot
3) medial foot 3) big toe
4) sole

reflexes Impaired knee jerk Impaired ankle jerk

1) 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 & SI root irritation).

2) 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

155
 Investigations

1. Plain x ray:
- AP and lateral views
- Dynamic study ( neutral, flexion, extension )
1) Narrowing of the disc space
2) Osteophytes
3) Obliteration of lumbar lordosis
4) Scoliosis

- To exclude other pathologies as metastatic lesions

2. MRI: the best diagnostic method in lumbar disc prolapse

3. CT scan: It detects:
1) lumbar canal stenosis 2) hypertrophied facet joint 3)narrow canal dimension.
4. 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, oblique ) views.
- Disc prolapse causes…
1) a filling defect in the theca
2) and obliteration or displacement of nerve root sleeve of the affected disc level
3) or complete block of the dye

5. Nerve conduction velocity & EMG: It will yield precise information on root lesion

Treatment

1. 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 and Muscle relaxants

5) Reduction of body weight and health education

156
2. Methods of surgical treatment:
❖ Indications:
1) Failure of non-surgical treatment.

2) Urgent surgery:

a) Cauda equina syndrome. b) Progressive motor deficit.

c) Severe, unremitting, leg pain which is not relieved by conservative measures.

 Trans-canal approaches:
1) Standard open laminectomy and discectomy
2) Microdiscectomy 3) Endoscopic discectomy
 Intra-discal procedures in selected patients
1) Automated percutaneous lumbar discectomy ( nucleotome )
2) Percutaneous endoscopic discectomy.
3) Laser disc decompression
4) Chemonucleolysis

Cauda equina syndrome

Low back pain and bilateral sciatica
❖ Motor ( LMNL ):
1) Bilateral weakness of dorsi and plantar flexion of the foot.
2) Weakness of hip flexor and/or extensors
3) Weakness of knee flexors and/or extensors may also occur.

❖ Sensory:
1) hypoesthesia bilaterally according to the spinal roots affected
2) saddle shaped hypoesthesia.

❖ Reflexes: ankle reflex is lost bilaterally & also may be the knee reflex.
❖ Autonomic:
1) sexual dysfunction → impotence
2) sphincteric disturbance:
1. retention or incontinence of urine, 2.diminished anal tone
3. chronic constipation or incontinence of stools
❖ Clinical test: SLRT → positive bilaterally
157
 Lumbar canal stenosis

Types

1. Congenital: congenital narrowing of the lumbar spinal canal.

2. 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.
 Predispose to root and cauda equina compression from….
➢ a prolapsed disc,
➢ osteophytes
➢ thickened ligamentum flavum
➢ or hypertrophied facet joint.
❖ Congenital narrowing of the spinal canal aggravates the
effect of nerve root and/or cauda equina compression.

Clinical picture

1) Root pain and sense of heaviness of both lower limbs develops after standing or walking
 relieved by sitting or lying down ( neurogenic claudication pain ).
2) Neurological deficit, such as muscle weakness or sensory troubles are bilateral,
predominantly at one side.
3) In many cases, sphincteric function impairment maybe manifested.

Management

 Investigation: - Plain x ray: may suggest lumbar spinal stenosis,

- but CT scan & MRI: are required to establish the diagnosis.

 Surgical treatment: - wide laminectomy and root decompression.

- Facetectomy may be done in some cases ± fusion

158
 Lumbar spondylolisthesis

- Forward sliding of one vertebral body over the other.

- This usually occurs between L5- SI and L4-L5.
- Displacement is due to:
1) congenital defective facet articulation,
2) fracture pars interarticularis ( isthmic spondylolisthesis )
3) or prolonged degenerative process of the spine ( degenerative spondylolisthesis )

- Narrowing of the spinal canal may cause root compression.

Treatment

1. Conservative:
1) External spinal support.
2) Analgesics.
3) Weight reduction.

2. 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

159
 INABILITY TO WALK

❖ Walking needs integration between:

{ CNS & Muscles & Skeleton } +/- Training

I- Central causes:
a- Brain:
1) CP 2) MR 3) Hydrocephalus
4) Cong. malformations
5) Brain damage ( tumors, infections)

b- Spinal cord:
1) Congenital → spina bifida.
2) Traumatic → spinal cord trauma.
3) Inflammatory → Pott’s disease of the spine.
4) Neoplastic → spinal cord tumors.

c- Anterior horn cells:

1) Poliomyelitis.
2) Spinal muscle atrophy. ( Werding - Hoffman disease )

d- Peripheral Nerve:
1) Guillian - Barre syndrome..
2) Polyneuritis (Diphtheria, Drugs,...).

e- Neuro muscular junction ( NMJ ) :

1) Botulism
2) Organophosphorus poisoning. BOM
3) Myasthenia gravis.

183
II- Muscular causes:
a) 1ry muscle disorders: Myopathies, Metabolic, Myositis.
b) 2nd muscle disorders: Rickets & malnutrition.

III- Skeletal: ( Bones, Joints )

a) Trauma ( to L.L. )
b) Rickets
c) Inflammation ( arthritis, osteomyelitis )

D.D. of inability to walk

1ry 2nd
The child has not walked before The child has walked before

1) Poliomyelitis.
1) Early poliomyelitis.
Paralytic 2) Post ( diphtheric, encephalitic or
2) Early paralysis before walking.
causes meningitic ) paralysis.
3) Cerebral palsy.
3) Cerebro -vascular accidents.

1) Rickets 1) Rickets
Non-
paralytic 2) MR 2) malnutrition
causes
3) Simple delayed walking 3) fractures or osteomyelitis

184
 Floppy infant

Definition: Infant with sever persistent hypotonia present at birth and in early
infancy

Floppy infant: - Central - Peripheral

Central features Peripheral features

[ Brain + spinal cord ] [ AHC, peripheral nerve, muscle, NMJ ]

1) Depressed level of consciousness 1) Baby is alert

2) Dysmorphic features
3) Predominantly axial muscle affection
4) Abnormal development or delayed
milestone
5) Reflexes: normal or even hyper-
reflexia
2) Normal facies
3) Poor feeding, may involve respiratory
muscles
4) More affection of distal muscles
5) Reflexes: hypo- or a- reflexia
❖ N.B: fasculation may be seen

❖ In neonate: the following suggestive of central hypotonia:

1) Early seizures 2) Apnea
3) Abnormal eye movement
4) Exaggerated irregular breathing pattern
❖ In infant: the following suggestive of central hypotonia:
1) Fisting of hands beyond first few month of life
2) Scissoring of legs on vertical suspension
3) Hyper-reflxia

❖ Central causes:
1) HIE
2) Brain insults: IVH
3) Chromosomal anomalies: DOWN syndrome
4) IEM and neuro-metabolic syndrome
185
❖ Peripheral causes:
1) AHC: spinal muscle atrophy
2) neuromuscular causes:
a) transient acquired neonatal myasthenia
b) infantile botulism

3) muscle causes: congenital muscular or myotonic dystrophy

Diagnosis

1- Detailed history:
1) Family history

2) Prenatal: - amount of fluid - polyhydramnios - breech presentation

3) Perinatal: - exposure to toxins - APGAR score - sepsis - time of floppiness

4) Neonatal history

2- Physical examination:
1) Dysmorphic features.. Syndromes

2) Weak cry, weak suckling, respiratory difficulties

3) Head lag

4) Ventral suspension → inverted U letter appearance

5) Vertical suspension → shoulder slipping through your

hands, hanging limbs
6) On laying supine:

➢ Flat occiput
➢ Flexed elbow
➢ Frog leg positon

7) Don’t forget: Reflexes - tongue fasculation

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3- Investigations:
1) Rule out systemic causes: sepsis, electrolytes disturbance
2) Rule out congenital infections: TORCH

❖ IF hypotonia is considered central:

1- Karyotyping
2- Inborn error of metabolism work up
3- Brain imaging

❖ IF hypotonia is considered peripheral:

1- Creatin kinase
2- NCV, EMG
3- DNA testing → SMA
4- Muscle biopsy

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 MENTAL HEALTH AND SUBSTANCE ABUSE

Some definitions

❖ Mental health:
- The World Health Organization (WHO) defines mental health as "a state of well-being in
which the individual:
➢ realizes his or her own abilities
➢ can cope with the normal stresses of life
➢ can work productively
➢ is able to make a contribution to his or her community"

❖ Mental disorder ( mental illness or psychiatric disorder ):

- is a behavioral or mental pattern that causes significant distress or impairment of
personal functioning.

- Such features may be persistent, relapsing and remitting, or occur as a single episode.

- Mental disorders comprise a broad range of problems, with different symptoms.

However, they are generally characterized by some combination of abnormal thoughts,
emotions, behavior and relationships with others.
 Examples are:
1. depression 2. anxiety disorders 3. schizophrenia
4. intellectual disabilities 5. disorders due to drug abuse

Importance of Mental Health:

1) It affects how we think, feel, act.

2) It also helps determine how we…
➢ handle stress
➢ relate to others
➢ make healthy choices.

3) It is important at every stage of life, from childhood & adolescence through adulthood.

232
 Benefits of Good Mental Health

1) A Stronger Ability to cope With Life's Stressors.

2) A Positive Self-Image.
3) Healthier Relationships.
4) Better Productivity.
5) Higher Quality of Life.

Risk Factors of Mental illness and Substance Abuse:

- Both substance use disorders & other mental illnesses are caused by overlapping
factors such as….
➢ genetic and epigenetic vulnerabilities,
➢ issues with similar areas of the brain,
➢ environmental influences such as early exposure to stress or trauma.

- Although the precise cause of mental illness isn't known, certain factors may increase risk
of developing mental health problems, including:

1) Genetic predisposition: Genetics play an important role in determining

2) vulnerability to most major psychiatric disorders, however not all who inherit the
gene will manifest the illness.

3) Age: Prevalence of mental illness varies with age…

➢ with common mental illnesses and substance abuse increasing from
adolescence through adulthood
➢ while depression and dementia are seen in old ages.

4) Sex: The overall prevalence of mental and behavioral disorders doesn’t seem to be
different between men and women…
➢ Anxiety and depression are more common among women
➢ while substance abuse is more common among men.

233
5) Diet:
➢ Poor quality diet high in saturated fat, refined sugar and processed foods
increase risk of depression and anxiety in children and adolescents.
➢ Deficiency in vitamin B and protein deficiency in Kwashiorkor have effects on
mental health.

❖ Substance use disorders (SUD) can often occur alongside eating disorders
including:
1. anorexia nervosa
2. bulimia nervosa
3. binge eating disorder

6) Infections: Parasites such as: - schistosomiasis - malaria - encephalitis

cause epilepsy and meningitis.

7) Toxic substances as alcohol and opiates.

8) Social determinants: the main “core” social determinants of mental health are:

1. racial discrimination and social exclusion

2. adverse early life experiences
3. poor education
4. unemployment
5. under-employment and job insecurity
6. poverty
7. income inequality
8. neighborhood deprivation; poor access to sufficient healthy food
9. poor housing quality.

1) Family, social networks, peer pressure are key influences of substance abuse
among adolescents.

234
 How are mental health and substance abuse related?

- Mental health problems and substance use disorders sometimes occur together.

- More than one in four adults living with serious mental health problems also has a
substance use problem.

- This is because:

• Certain illegal drugs can cause people with an addiction to experience one or more
symptoms of a mental health problem.

• Mental health problems can sometimes lead to alcohol or drug use, as some people
with a mental health problem may misuse these substances as a form of self-
medication.

• Mental and substance use disorders share some underlying causes, including…
➢ changes in brain composition
➢ genetic vulnerabilities
➢ early exposure to stress or trauma

Prevalence and Burden of Mental illness & Substance Abuse:

- Mental health problems are one of the main causes of the overall disease burden
worldwide. However, mental health disorders remain widely under-reported.

- About 14% of the global burden of disease is attributed to mental disorders.

- The burden of mental disorders is likely to have been underestimated because of

inadequate appreciation of the inter-play between mental illness and other health
disorders.

- WHO indicates from a survey of 26 countries that depressive disorders and anxiety
disorders are the most common globally ( Common mental disorders ), whereas
substance and impulse-control disorders are consistently less prevalent.

- The number of persons with common mental disorders globally is going up, particularly
in lower-income countries, because…
➢ the population is growing
➢ more people are living to the age when depression & anxiety most commonly occurs.
235
- In Egypt:

➢ Neuropsychiatric disorders are estimated to contribute to 15.1% of the burden of

disease
➢ the suicide rate is estimated at 1.7 per 100 000 per year.
➢ Depression, anxiety, drug use disorders rank among the top 25 causes of burden
of disease (World Health Organization, 2015).

- Estimates of drug users in Egypt range from 1 million to 6 million people, with most drug
users being in the 15-25 age groups.

- Accurate statistics are difficult to obtain because of the stigma associated with being an
addict.

- The high prevalence rates of mental health disorders is an important concern also for
public health professionals because of the many consequences for individuals and their
families, as well as the socioeconomic burden on national economies.

- The direct death from mental health and substance use disorders is typically low.
However, mental health disorders are also associated with significant number of indirect
deaths through suicide and self-harm.

- It is projected that, by 2030, mental health problems ( particularly depression ) will be

the leading cause of mortality and morbidity globally.

The impact of Mental Illness and Substance Abuse on Individuals,

Families, and Communities as well as on Quality of Life:

- Mental illness is a leading cause of disability

- Untreated mental illness can cause: severe emotional, behavioral, physical health
problems

- Drug abuse is often accompanied by a devastating social impact upon community life.

236
❖ Complications include:
a. At individual level:
1) Unhappiness and decreased enjoyment of life.

2) Increased absenteeism from work or school

3) Legal and financial problems.

4) Self-harm and harm to others, including suicide or homicide

5) Alters neuromuscular coordination, reaction time and judgment and increase

accidents.

6) Weakened immune system.

7) Heart disease and other medical conditions.

8) Social isolation.

9) Problems with tobacco, alcohol and other drugs.

b. At family level:
1) Family conflicts.

2) Relationship difficulties

c. At community level:
1) Decline in quality and quantity of work products.

2) Increase money expenditure for treatment of abusers.

3) Increased crime and violence.

4) Increased morbidity, withdrawal symptoms and premature death due to over dose
intake.

5) Poverty and homelessness.

237
 Prevention of Mental Illness and Substance Abuse:

a. Primordial Prevention:
- To reduce the health, social and economic burdens of mental disorders
it is essential that countries and regions pay greater attention to prevention of mental
health at the level of:
➢ policy formulation
➢ legislation
➢ decision-making
➢ resource allocation within the overall health care system.

- Primordial prevention targets the underlying stage of natural disease by targeting the
underlying social conditions that promote disease onset.

b. Primary Prevention:
- There must be a national plan for mental health services, develop human resources
and integrate mental health with general primary health care.

1) Mental health promotion:

 improving the ability of people to deal more effectively with everyday life
stresses.
 Mental health education courses to improve mental abilities through:
➢ life skills education,
➢ skills for interpersonal communication and stress management
➢ with special programs directed to vulnerable groups:
{ children, adolescents, youth , the elderly }

2) Education, employment, social well-being, availability of food, housing

and other public health-related factors: play an important role in preventing
mental disorders and promoting mental health.

3) Raising public awareness about mental health disorders…

Patients need treatment and kind care rather than punishment.

4) Encourage youth for physical exercise and safe recreation activities.

238
c. Secondary Prevention:
1) Early detection of mental disorders/illness & substance abuse in primary health care:
➢ Screening:
• for early detection of mental illness and substance abuse at nursery, school,
university, military and work.

• A multi-sector cooperation is necessary to screen different groups.

➢ Early diagnosis:
• the progression from asymptomatic to symptomatic mental health disorder is
subtle.

• Mental disorder may exist for longer periods till recognized.

• Early diagnosis needs capacity building of lay person, other professionals and
general practitioners.
2) Proper management and/or referral to psychiatrist: Include..
➢ Hot line service for rapid management and confidential service.
➢ Complete psychiatric assessment for proper diagnosis of cases.
➢ Counseling, psychotherapy and medical treatment.
➢ Admission to psychiatric word/hospital.

d. Tertiary Prevention:
- It includes interventions that reduce disability and all forms of rehabilitation as well as
prevention of relapses of the illness.

- The integration of needy groups in the society is needed.

- It can be achieved by:

1) Increasing society understanding of the causes of disabilities and the abilities of

the needy/disabled group.

2) Attempting to reverse peoples and children negative attitudes.

3) Improving health-workers approach toward needy/disabled groups.

4) Improving the self-esteem and confidence of needy/disabled groups.

5) Showing needy/disabled groups can take care of others, not just themselves.

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 6) Increasing opportunities for physical and socio-economic integration of
needy/disabled groups in daily activities.

7) Presenting the abilities of needy/disabled groups through public information

campaigns to reduce stigmatization of mental problems.

8) Training the health workers about the needs of special groups.

9) Providing facilities/ services- day care centers and counseling sites to families of
needy/disabled.

10) Orientation of children about disabilities in schools, helping regular schools

integrates disabled children and promotes inclusive education.

11) Communicate to parents about disabilities of their disabled children.

12) Improve physical accessibility to public places, like mosques, governmental

offices and schools.

13) Create incentives for employers to hire disabled people.

Mental Health Program in Egypt:

- The WHO country office supports the Ministry of Health and Population in integrating
mental health services into primary health care and raising awareness in schools and
universities to reduce the stigma of mental health illnesses.

- In Egypt the national mental health program focuses on:

1) Decentralization of mental health care and community care in different governorates.

2) The inclusion of mental health in primary health care.

3) Training of family doctors to deal with the main mental disorders.

4) Awareness-raising among the public regarding recognition of mental disorders and

methods of referral.

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 SUBSTANCE USE DISORDERS

Definition

- Dependence ( related words, addiction ):

➢ Psychological: Craving ( intense desire ) for the substance to avoid dysphoric state.

➢ Physiological ( physical ): Altered physiologic state from repeated use of the

substance, its cessation results in a specific syndrome.
➢ Behavioral: maladaptive pattern of substance seeking activities.

- Tolerance: after repeated use, a decreased effect occurred and a larger dose is needed
to get the previous effect.

- Abuse: Use of any drug ( usually self-administration ) that is deviated from approved
social or medical patterns, while misuse (usually applied to prescribed drugs),

- Substance Misuse: Similar to abuse but usually applies to drugs prescribed by

physicians that are not used properly.

- Intoxication: Specific syndrome due to large dose of a substance.

- Withdrawal: Specific syndrome due to stoppage or reduction of the amount of a

substance after prolonged use.

Epidemiology

- The most recent National Survey on Drug Use by the Substance Abuse and Mental Health
Services Administration ( SAMHSA ) in 2019 estimates that…

➢ 20.2 million Americans ( 7.4% ) had a substance or alcohol abuse or dependence

disorder.
➢ Up to 50% with comorbid psychiatric disorder,
➢ about 35-60% with comorbid diagnosis of antisocial personality disorder.

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 Etiology: biopsychosocial Model; bio ( genetic, biological, Psychosocial )

1. Genetic factors:
- Strong in alcohol abuse by twin studies, less conclusive data in other substances.

- In a study, genes that affect dopamine production have been postulated.

2. Biological:
- as too little endogenous opioid activity ( low endorphins ) may be with risk for opioid
dependence.

- Also, major neurotransmitters are possibly involved in substance abuse as dopamine

and GABA.

3. Psychosocial: Learning and conditioning:

a) Learning from family members. Also, family problems, poverty and underlying
depression are risk factors.
b) Positive reinforcement, as:
➢ euphoric state
➢ alleviation of pain, anxiety, depression.

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 I. ALCOHOL RELATED DISORDERS
ALCOHOLS TOXICITIES

Ethyle Alcohol ( Ethanol )

Acute Toxicity of Ethanol

Sources

1) Ethanol is derived from fermentation of sugars in ( fruits, cereals, vegetables )

2) it presents in alcoholic beverages ( as beer, wine, champagne, whisky, vodka )

3) it is used in hundreds of medicinal preparations as solvent in concentrations

ranging from [ 0.3 - 75% ]

4) Household products ( mouthwashes, colognes and perfumes ) which may contain

up to 70 % ethanol

Mode of acute toxicity:

- Ethanol is the most frequently ingested toxin throughout the world.

- Intentional and accidental are due to the availability of household products.

Toxic dose: - Adult: 5 gm / kg - Children: 3 gm / kg

Toxicokinetics

- It is rapidly absorbed from GIT within 30 to 60 minutes:

➢ 20% from the stomach
➢ the remainder 80% from small intestine.
- It's metabolized mainly by alcohol dehydrogenase enzyme to acetaldehyde and then
aldehyde dehydrogenase to oxidize acetaldehyde to acetate which becomes acetyl
coenzyme A.

243
 Pathophysiology

- Ethanol itself and its metabolite acetaldehyde affect every organ system in the body.

Clinical presentation

- Ethanol is a CNS depressant; it has variable effects on individuals depending on blood

ethanol level (Table 1).

Blood
Clinical signs and symptoms
ethanol

- Euphoria - Sense of warmth - Sense of well-being

- Talkativeness - Loss of inhibitions
25 - 50
- Impaired judgment and control
mg/dl
- loss of self-confidence - Increased reaction time
- Impaired fine performance.

- Excitement - Emotional instability - Impaired judgment

50 - 100
- Poor memory and comprehension - Increased reaction time
mg /dl
- Slurred speech - Impaired balance-Ataxia

- Drowsiness - Confusion - Disorientation

100 - 250 - exaggerated emotional states - Nausea & vomiting

mg /dl - Altered sensation, perception and balance
- Slurred speech, ataxia and muscular incoordination

- Apathy - stupor - decreased response to stimuli

250 - 400
- significant muscular incoordination
mg /dl
- Vomiting - Incontinence of urine and feces

- Coma - respiratory paralysis - decreased or absent reflexes

400 - 500 - constricted pupil, which dilate with painful stimulation

mg / dl [ +ve McEwan's sign ]
- hemodynamic and respiratory instability - Possible death.

244
 In experienced drinkers much higher levels may be
required to produce significant depression of the
central nervous system.

Diagnosis

- The diagnosis is based on:

➢ history of ingestion,
➢ altered mental status
➢ high blood alcohol concentration
➢ characteristic odor in the mouth.

Laboratory investigations

1) Blood and urine ethanol level:

 by immunoassay or gas chromatography is commonly used for determination of

ethanol in liquid specimens.

2) Bedside breath alcohol analysis ( breathalyzers or drunkometer ):

 It is a useful, inexpensive screening tool that can be used in the emergency setting
using exhaled air ethanol analyzers

3) Serum glucose level.

4) Arterial blood gases and serum electrolytes.

Differential diagnosis

- Both acute ethanol toxicity and atropine toxicity share…

➢ hallucinations
➢ flushing
➢ unsteady gait
➢ abnormal movements
 but can be differentiated by the following items (Table 2):

245
 Items Acute alcohol toxicity Atropine toxicity

smell of the
Smell of alcohol No characteristic smell
breath

Changeable
( constricted pupil, which dilate
Pupils Fixed dilated
with painful stimulation)
[ +ve McEwan's sign ]

Skin Flushed and sweating Hot and dry

Temperature Subnormal High ( atropine fever )

Vomiting Possible No vomiting

Speech Slurred speech Hoarseness of voice

Movement Tremors Purposeless movements

Chemical Detection of ethanol in blood and

Detection of tropic acid in urine
analysis breath

Treatment

1) Treatment begins with evaluation of the patient's level of:

- consciousness - airway patency - adequacy of ventilation.

2) Altered mental status:

➢ Glucose ( 1-2 ml / kg of dextrose 5 % ) to correct hypoglycemia
➢ Thiamine (100 mg IV) will treat and prevent Wernicke's encephalopathy.

3) Decontamination:
 Gastric lavage indicated if ethanol ingestion has occurred within 30 minutes
because ethanol is rapidly absorbed.

4) Elimination:
 Hemodialysis in patients with high blood alcohol concentration > 500mg/ dl

5) Symptomatic:
➢ Correct dehydration, electrolytes and acid-base imbalance
➢ Warming for hypothermia.
246
 Methyl Alcohol Toxicity (Methanol)

Sources

- Methanol ( methyl alcohol or wood alcohol ) is widely used as:

1. antifreeze 2. remover for paints and varnishes

3. fuel 4. household solvents

5. industrial solvent 6. manufacture of formaldehyde.

Toxicokinetics

- Absorption occurs via the GIT, dermal, respiratory routes;

 with peak GIT absorption occurring 30 to 60 minutes post ingestion.

- Hepatic conversion to formaldehyde via alcohol dehydrogenase and then metabolism to

formic acid and formate causing metabolic acidosis.

- Small amounts of methanol are eliminated unchanged via the respiratory & renal routes

Pathophysiology:

- The parent alcohol, methanol can cause:

➢ CNS depression
➢ produced decreased cardiac output, stroke volume and systemic blood pressure.

- Formaldehyde is rapidly metabolized to formic acid ( formic acid is responsible for the
metabolic acidosis and ocular toxicity ).

247
 Diagnosis

a. History of exposure to either source of methanol.

b. Clinical presentation:
1. Central nervous depression: Include…
- Dizziness - headache - agitation - stupor
- coma - seizures - cerebral edema
- and infarcts or hemorrhages of basal ganglia.

2. Ocular toxicity:
❖ Symptoms:

- Blurred vision ( cloudy vision ) - photophobia - decreased visual acuity

- visual hallucinations ( snowstorm, dancing spots or flashes )
- partial to total blindness.

❖ Signs:

- Sluggish or nonreactive pupils - papilledema

- hyperemia of optic nerve disc - retinal edema or hemorrhages.

3. Cardiopulmonary: Tachycardia or bradycardia & hyperpnea.

4. Gastrointestinal:
- Nausea, Vomiting, Anorexia, abDominal pain,

- gastritis and pancreatitis.

Laboratory investigations

1) Blood methanol level; A level of 20 mg/dL or more is considered toxic, even in the
absence of acidosis.
2) ABG & electrolytes levels
3) Blood glucose & lactate
4) Electrocardiogram (ECG).
5) Chest radiograph: recommended in patients with suspected aspiration or
pulmonary edema
248
 Treatment

1. General: Supportive care, including…

1) ( appropriate airway - intravenous access - cardiac monitoring )
2) Sodium bicarbonate IV for life-threatening metabolic acidosis
3) Calcium IV for symptomatic hypocalcemia
4) Treat seizures with benzodiazepines and phenobarbital.

2. GI decontamination: for large oral ingestions.

3. Antidote ( Alcohol dehydrogenase inhibitor ):

1) Fomepizole ( 4- methylpyrazole ):
 Potent inhibitor of alcohol dehydrogenase enzyme preventing formation of toxic
metabolites.
2) Ethanol:
 Monitor serum ethanol level every 1-2 hr until steady state level of 100-150 mg/dL
is achieved, also monitor for CNS depression
 Administer ethanol or fomepizole until…
➢ methanol level is below 20 mg/dL &
➢ metabolic acidosis has corrected.

4. Hemodialysis: ( Eliminate toxic metabolites ) …effective in specific indications

5. Cofactors: Folinic acid ( leucovorin )

- It enhances metabolism of formic acid to carbon dioxide & water via folate dependant
pathway.

6. Sequelae:
- Permanent ophthalmologic ( diminished vision, visual field defects, irreversible loss of
vision) and neurologic sequelae.

249
 Isopropyl Alcohol (Isopropanol)
Sources

- Isopropyl alcohol is used widely as [ a solvent, an antiseptic, a disinfectant ]

- It is often ingested by alcoholics as a cheap substitute.

Pharmacokinetics

- It is well absorbed within 2 hours and rapidly distributed.

- It metabolized to acetone by alcohol dehydrogenase enzyme.

Mechanism of toxicity: ( more potent CNS depressant than ethanol ).

- It is a potent CNS depressant.

- Toxic effects caused by parent agent rather than its metabolite acetone which may
prolong CNS depression.

- Myocardial depression and hypotension in very large doses.

Treatment: Emergency stabilization and supportive measures.

Ethylene Glycol

Sources

- It is the primary ingredient (up to 95%) in antifreeze. It sometimes is consumed

intentionally as an alcohol substitute by alcoholics.

- Ethylene glycol is well absorbed, metabolized by alcohol dehydrogenase to

[ glycoaldehyde, then to glycolic, glyoxylic, oxalic acids ]

- Intoxication causes mild gastritis; and its metabolic products cause metabolic acidosis,
renal failure, and death.

Treatment

1) Emergency stabilization and supportive measures

2) antidotes:( fomepizol and ethanol ) 3( hemodialysis for severe cases

250
 Alcohol use disorders
( with chronic alcohol addiction )
1. CNS:
a) Alcohol induced amnestic disorder:
➢ Wernicke's encephalopathy ( Acute symptoms )
➢ Korsakoff's syndrome ( chronic condition )….. With:
- Anterograde amnesia - impaired recent memory - confusion
- vestibular dysfunction - horizontal nystagmus - lateral ocular palsy
- sluggish reaction to light and ataxia.

❖ Treatment: Thiamine.

b) Alcohol pellagra encephalopathy: with…

- confusion - insomnia - irritability even delirium
❖ Treated with: niacin

c) Alcohol induced dementia:

- partially or completely reversible during the 1st year of abstinence.

d) Alcohol related psychotic disorder:

- about 3% experience auditory hallucinations or paranoid delusions with heavy drinking

- Also, there is alcohol induced mood disorder ( MDD, 80% of alcoholics report history of
depression ) & alcohol induced anxiety & sleep disorders.

2. Blood: as…
- anemia - leukopenia and thrombocytopenia
- Also: hyponatremia & hypomagnesaemia & hypoglycemia

3. Cardiovascular:
- Myocardial infarction risk, increased blood pressure with risk of cerebrovascular disease

4. Alcoholic hepatitis, hepatic cirrhosis, fatty liver, liver damage.

5. GIT: esophagitis, gastritis & gastric ulcers.

6. Increased incidence of cancer: ( esophageal, clonic, hepatic, lung ).

7- Dermatological: Skin itching.

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 Alcohol withdrawal symptoms:

1. CNS:
- fever - mydriasis - anxiety - insomnia
- psychotic symptoms ( delusion, hallucination ) - seizures & delirium tremens.
2. Cardiovascular: Tachycardia, hypertension.

3. GIT: Nausea, vomiting.

4. Peripheral:
- Tremors - sweating - facial flushing - shakes
- psychomotor activity ranging from hyperexcitability to lethargy.
❖ Untreated delirium tremens ( DTs ): has a mortality rate of 20%.

Treatment

1) BZ ( in a rapidly reducing way ) is the treatment of choice

 as chlordiazepoxide and diazepam: They exhibit cross - tolerance with alcohol
and have anticonvulsant properties
 also, carbamazepine may be used for seizures.

2) Antipsychotics as haloperidol ( in a tow dose ) are useful in managing delusions and

hallucinations.

3) Thiamine: A minimum 300 mg daily is needed during alcohol withdrawal ( for about 5
days ) and periods of continued intake ( IV or IM at the beginning due to poor GIT
absorption).

4) B-blockers & clonidine: have also been used to block sympathetic hyperactivity

5) Metoclopramide: 10 mg /4-6 hours for nausea and vomiting.

6) Loperamide: for diarrhea.

7) Paracetamol: for pain.

8) Also, ensure adequate fluid intake to maintain hydration & correct any electrolyte
imbalance.

9) Rehabilitation: aimed at abstinence and treatment of comorbid psychopathology.

252
 Relapse prevention (maintenance):

- With Acamprosate, disulfiram, naltrexone and naltrexone depot.

1. Acamprosate:
- it is a glutamatergic NMDA antagonist and also increases GABA function.

- Dose: 666 mg 3 times daily.

2. Disulfiram:
- It inhibits aldehyde dehydrogenase with accumulation of a toxic product acetaldehyde
( if the patient drink alcohol ), with resultant adverse reactions.

- Dose: 800 mg for the first dose, reducing 100-200 daily for maintenance.
3. Naltrexone:
- Opioid blockade ( a non-selective opioid receptors antagonist ), prevents increased
dopaminergic activity after the consumption of alcohol (as alcohol act on opioid
receptors leading to dopamine release), thus reducing its rewarding effect (pleasure)
and craving.

- Dose 50 mg/day.

❖ Naltrexone depot: 380 mg/4weeks IM gluteal injection.

4. Rehabilitation: aimed at abstinence & treatment of comorbid psychopathology.

 Alcoholics Anonymous:

• is a 12-step plan in order to overcome addictions & compulsions.

• The basic premise of this model is that people can help one another to achieve &
maintain abstinence from substances of abuse.

• Self-help group during inpatient or outpatient rehabilitation.

 Psychotherapy:

a) Individual therapy: therapists focus on the dynamics leading to opiate use, the
perceived positive effects of the opiate, & find other ways to achieve these effects.
b) Family therapy: focus on changes in the family's activities that may help the
patient stay off the drug & direct energies in different directions.
This approach can be used on an outpatient basis.

253
 SCHIZOPHRENIA

Definition

- Psychosis: is characterized by…

➢ impaired reality testing ( inability to distinguish reality from fantasy )
➢ with specific psychotic symptoms like ( delusions, hallucinations )
- Schizophrenia:
➢ is a clinical syndrome of variable but profoundly disruptive psychopathology that
involves ( cognition, thinking, perception, emotion, and behavior)
➢ in which patients have psychotic symptoms and social or occupational dysfunction
that persists for at least 6 months.

- Usually before the age of 25, persists throughout life, affects persons of all social classes.

Epidemiology

- Lifetime prevalence: Affects 1% of the general population.

- Sex: males = females. - Geographical: Urban > Rural.

- Age: → males have onset earlier than females, males ( 10-25 ys ).

→ females have bimodal onset ( 25-35 ys and > 40 ys ).

Etiology

1. Neurotransmitter theory:
A. Dopamine hypothesis: Schizophrenia is due to hyperactivity in brain
dopaminergic pathways…. This theory is consistent with:
1) The efficacy of antipsychotics ( dopamine receptor antagonists ).
2) The ability of some drugs like amphetamine that stimulate dopaminergic activity to
induce psychosis.
3) Presence of higher levels of dopamine receptors in subcortical nuclei of
schizophrenics

B. Serotonin hypothesis: Excess serotonin → +ve & -ve symptoms. Evidenced by

the efficacy of serotonin-dopamine antagonists in reducing psychotic symptoms.

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2. Genetic theory:
- Increase the incidence of schizophrenia in subjects related to an affected person.

1) General population → 1 %
2) Siblings of affected subjects → 8%
3) Off-springs of one affected parent → 12%
4) Dizygotic twin of schizophrenia Pt → 12%
5) Off-springs of two affected parents → 40%
6) Monozygotic twin of schizophrenia Pt → 47%
7) Defects in: short arms of chromosomes 6, 8 & 10 & long arms of chromosome 1, 5, 6,
13, 15,22.

3. Brain structural theory:

- Loss of the brain volume due to decrease density of axons, dendrites and synapses.

- Imaging techniques showed..

➢ decreased size
➢ impaired function in limbic system and frontal lobes.

4. Psychosocial theory:
- Families with overt criticism, hostility, and over-involvement toward schizophrenia
patients ( families with high Expressed Emotion ).

Diagnosis

A. Two or more of the following must be present:

1) Hallucinations: auditory hallucinations are the most prominent type, but other
types like [ visual, tactile, olfactory, gustatory ] may be present.

2) Delusions:
1. persecutory 2. grandiose 3. paranoid
4. religious 5. reference 6. thought broadcasting
7. thought insertion 8. thought withdrawal

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 3) Disorganized behavior:
1. aggressive 2. agitated. 3. odd clothing or appearance,
4. odd social behavior 5. repetitive-stereotyped behavior
6. catatonic behavior:
- motoric immobility or stupor - excessive motor activity
- extreme negativism or mutism - echolalia or echopraxia.
- peculiarities of voluntary movements

4) Disorganized speech: 1. incoherent 2. clang association 3. neologism.

5) Negative symptoms:

1. Affective flattening or blunting, 2. poverty of speech ( alogia )

3. loss of volition 4. thought blocking,
5. poor grooming or social withdrawal.

B. The symptoms must last at least for 6 months.

C. Presence of significant occupational and /or social dysfunction.

D. The condition is not substance induced or due to general medical

condition.

Treatment

1. Hospitalization for:
1) Diagnostic purposes.
2) Stabilization of medication.
3) Patients with suicidal or homicidal ideation.
4) Grossly disorganized or inappropriate behavior.
5) Catatonic schizophrenia.
6) If ECT is indicated.

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2. Pharmacotherapy:
I. Typical antipsychotics [ Dopamine receptor antagonist ( DA ) ]:

• Mechanism of action:
 through blocking of dopamine receptors in mesolimbic-mesocortical pathway.

• Efficacy: effective in positive than negative psychotic symptoms.

• Examples: - trifluperazine - haloperidol - chlorpromazine - thioridazine.

• Side effects:

1) Acute dystonia: slow sustained contractions of the trunk or limbs.

2) Neuroleptic malignant syndrome:
- rigidity - hyperpyrexia - disturbed conscious level
- elevated CPK - leucocytosis
3) Parkinsonism.
4) Hyperprolactinaemia.
5) Orthosatic hypotension.
6) Dry mouth.
7) constipation.

II. Atypical antipsychotics: Serotonin and dopamine antagonists (SDA):

• Mechanism of action:
 Through blocking of serotonin receptors and dopamine receptors.

• Efficacy: Effective in both positive & negative psychotic symptoms.

• Examples: [ - Risperidone - olanzapine - clozapine - quetiapine ]

• Side effects:

1) Milder motor side effects.

2) But others (weight gain, diabetes).

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3. Elcetro-convuIsive therapy:
❖ Indications:
1) Acute schizophrenia especially paranoid, catatonic, prominent affective symptoms.
2) Treatment resistant schizophrenia
3) Considerable suicide risk.
- It is performed under general anesthesia.

- Acts through remodulation of brain neurotransmitters.

❖ Cessions:
- About 6-12 treatments.

- Done twice or three times weekly according to the disease and its severity.

4. Psychosocial therapy:
a) Behavior therapy:
 to reinforce the desired behaviors & minimize the undesired behaviors.

b) Group therapy: focusing on supporting and developing social skills.

c) Family therapy: to improve family dynamics.

Other Psychotic Disorders

1. Brief psychotic disorder: One or more of..

1) delusions 2) hallucinations 3) disorganized speech
4) disorganized or catatonic behavior
 Must be present for duration ranges from 1 day to 1 month.

2. Schizophreniform disorder:
- The same clinical manifestations as schizophrenia.

- Except the duration of schizophreniform disorder ranges from one month to 6 months.

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3. Delusional disorder:
- Non-bizarre delusions.

- At least one month’s duration… In the absence of other psychotic features.

4. Secondary psychotic disorders:

1) Psychotic disorder due to general medical conditions.
2) Substance-induced psychotic disorder.

5. Schizoaffective disorder:
- At some time, there is mood disturbance in the form of depressive episode or manic
episode, occur in the presence of schizophrenic symptoms.

- 2 weeks of delusions or hallucinations in absence of mood symptoms.

6. Postpartum psychosis:
- Syndrome occurs after childbirth (1st 4 weeks).

- Initial complaints of [ insomnia, restlessness, emotional lability ]

- Progress to confusion, irrationality, delusions and obsessive concerns about the infant.

- Thoughts of wanting to harm the baby or self are characteristic.

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