Peripheral Nerve Injury

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Peripheral Nerve Injury

• Loss of motor function, sensory
• function, or both
• may result from an injury to a peripheral nerve.

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• Cranial nerves
• Spinal nerves
• Nerves of the extremities
• Cervical, Brachial, and Lumbo-sacral Plexi

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Etiology

• Trauma
• Blunt eg wrong posture fracture
• - Penetrating wound or surgery
• Acute compression
• Electrical burn
• Chronic
• -Tight nerve passage
• -Tumors

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Structure of the nerve
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Pathophysiology

• Demyelination or axonal degeneration,result in
  disruption of the sensory and/or motor function
  of the injured nerve.
• WALLERIAN DEGENERATION 1 MM PER DAY
• Recovery occurs with remyelination and with
• axonal regeneration and reinnervation of the
  sensory receptors, muscle end plates, or both.
• Partial or complete interruption of normal
  physiology of the nerve.
• NERVE CONDUCTION IS AFFECTED.

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Pathophysiology

• Neuropraxia reversible failure of propagation of
  the electrical impulse across the affected nerve
  segment without anatomical disturbance of the
  nerve. eg Saturday night palsy
• Axonotemes is complete absence of sensory and
  motor activities. days-weeks axonal and myelin
  sheath damage loss of cell body continuity to
  its end organ. Endo , peri and epineurium are
  preserved. prognosis for recovery is good
• Neurotemes is complete disrubtion of all the
  axons and supporting connective tissue
  structures. very poor prognosis without surgical
  repair.

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Clinical

• Depends on the nerve affected
• Pain
• Loss of sensation
• Loss of movment
• Loss of reflexes
• Wasting
• Trophic changes (skin,sc,neurovascular,bones,mus
  cles)
• Contractures
• Causalgia

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Diagnostic aids

• X-ray
• EMG
• NCS
• MRI

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Treatment

• Medical therapy
• - protection of the joints muscle
• - Physical therapy
• Surgical therapy
• - Reconstruction of nerve continuity
• - Nerve graft
• - Nerve transfer
• Closed injuries conservative ??no evidence of
  recovery surgery is recommended.
• Open injury (laceration) Surgical exploration
  is recommended as soon as possible. (Crush
  injury) exploration may be delayed for 3 months
  surgical reconstruction with repair or graft is
  indicated.

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Raised intracranial pressure

• The major causes of raised ICP are haematomas,
  mass lesions, brain edema and hydrocephalus
• skull as a rigid container that encloses the
  brain, cerebrospinal fluid (CSF) and
  arterial/venous blood.
• Results in reduced cerebral perfusion and brain
  herniation

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Clinical features

• Symptoms of raised ICP in a patient include
  headaches that tend to be worse in the early
  morning or on lying down and may improve with
  ambulation. Associated symptoms include nausea,
  vomiting or visual disturbance, particularly
  double vision or blurred vision. The headache may
  be exacerbated by coughing, straining or bending.
  
• In addition there may be symptoms relevant to the
  location of the pathology, for example, cognitive
  and personality change, unsteadiness of gait and
  incontinence of urine in frontal lobe pathology
  or right-sided weakness and garbled speech in
  dominant temporal lobe pathology.
• As ICP increases further, relatives may report
  lethargy or drowsiness followed by
  unconsciousness and coma .
• Raised ICP may be associated with papilloedema on
  fundoscopy .There may also be diplopia due to a
  sixth nerve palsy this nerve is vulnerable to
  downwards cerebral shift of any cause due to its
  long intracranial course, sometimes called a
  false localising sign. There may be abnormalities
  of conjugate gaze.
• In infants Progressive macrocephaly , Bulging
  anterior fontanelle , Dilated scalp veins,
  Sun-setting eyes

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Child with sun-setting eye sign due to
hydrocephalus.
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Papilloedema showing a swollen optic disc with
blurred margins.
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Treatment

• Appropriate treatment of raised ICP depends on
  identifying the cause.
• Medical
• Mannitol is an osmotic diuretic that can be used
  in emergency settings to reduce ICP the dose is
  0.51.0 g kg.
• Vasogenic oedema is often treated with the
  administration of high-dose steroids in the form
  of dexamethasone, for example 8 mg twice daily.
  Steroids reduce the permeability of the
  bloodbrain barrier.
• A carbonic anhydrase inhibitor such as
  acetazolamide can play a role in control of
  raised ICP in idiopathic intracranial
  hypertension and acts by reducing CSF production.
• Surgical
• A variety of mass lesions can cause raised ICP
  and are amenable to surgical treatment via
  craniotomy
• in trauma, acute extradural and subdural
  haematomas, intracerebral contusions and chronic
  subdural haematomas
• in cerebrovascular pathology, superficial lobar
  haematomas, haematomas associated with ruptured
• aneurysms
• in neuro-oncology, a variety of primary and
  secondary tumours.

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HYDROCEPHALUS

• Hydrocephalus is a condition in which there is
  disequilibrium between CSF production and
  absorption, leading to raised ICP, and is often
  associated with dilated ventricles.
• CSF production is primarily by the choroid plexus
  of the ventricles and is an active process
  independent of ICP. Some CSFproduction occurs by
  transependymal spread through the ventricular
  walls from the cerebral extracellular fluid, and
  from the spinal dural nerve root sheaths.
• CSF flows from the lateral ventricles, through
  the foramen of Munro, into the third ventricle
  and then into the cerebral aqueduct and fourth
  ventricle before exiting into the subarachnoid
  space via the midline foramen of Magendie and
  lateral foramina of Lushka.
• CSF absorption is a pressure-dependent passive
  process involving filtration across the arachnoid
  villi, which are abundant along the superior
  sagittal sinus into which the CSF is absorbed.
• The total CSF volume in an adult is about 150 ml
  . CSF production occurs at a rate of 450 ml day,
  resulting in a turnover of three volumes per day

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Aetiology of hydrocephalus

• Obstructive hydrocephalus
• blocking the CSF pathways from the lateral
  ventricles to the fourth ventricle
• Susceptible sites include the foramen
• of Munro and cerebral aqueduct .
• Lesions within the ventricle
• Lesions in the ventricular wall
• Lesions distant from the ventricle but with a
  mass effect
• Communicating hydrocephalus
• Post haemorrhagic
• CSF infection
• Raised CSF protein
• Excessive CSF production (rare)
• Choroid plexus
• papilloma/carcinoma

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Investigation

• Lumbar puncture is contraindicated in obstructive
  hydrocephalus because of the risk of causing
  tonsillar herniation and death.
• Ventricular size can be assessed with a
  computerised tomography (CT) scan of the brain
  (Fig. 40.6).
• A magnetic resonance imaging (MRI) scan of the
  brain can provide better anatomical detail of
  lesions causing hydrocephalus and is particularly
  useful in the diagnosis of aqueduct stenosis.
• ICP monitoring with a parenchymal probe placed
  into the frontal lobe via a twistdrill burrhole
  is a useful diagnostic tool for patients in whom
  hydrocephalus or CSF shunt dysfunction is
  suspected.

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Management

• Management of hydrocephalus will depend on the
  underlying cause. Options include removing a
  causative mass lesion, ventricular shunting or
  third ventriculostomy.
• Removing a causative mass lesion
• Intracranial mass lesions may present with
  obstructive hydrocephalus
• Ventriculoperitoneal shunt
• A ventriculoperitoneal shunt involves the
  insertion of a catheter into the lateral
  ventricle (usually right frontal or occipital).
  The catheter is then connected to a shunt valve
  under the scalp and finally to a distal catheter,
  which is tunneled subcutaneously down to the
  abdomen and inserted into the peritoneal cavity.
• If the CSF pressure exceeds the shunt valve
  pressure, then CSF will flow out of the distal
  catheter and be absorbed by the peritoneal
  lining.
• Other options for distal catheter placement
  include the right trium via the deep facial and
  jugular vein (ventriculo-atrial shunt) or the
  pleural cavity (ventriculopleural shunt).

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cerebrospinal fluid shunt.
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Shunt complications

• The most common complications include shunt
  blockage and infection.
• 1-Shunt blockage may affect the ventricular
  catheter, shunt valve or distal catheter.
• Causes of blockage include choroid plexus
  adhesion, blood, cellular debris or misplacement
  of the distal catheter in the pre-peritoneal
  space.
• More than one-half of cases of shunt blockage are
  subsequently shown to be infected.
• 2- Shunt infection affects between 1 and 7 of
  shunt insertions and is usually caused by skin
  commensals, such as Staphylococcus epidermidis
• Most infections become apparent clinically by 6
  weeks and over 90 are apparent within 6 months.
• Treatment is by removal of the shunt, external
  CSF drainage and treatment of infection prior to
  re-insertion of the shunt at a different site.
• The introduction of antibiotic-impregnated
  catheters has resulted in a reduction in shunt
  infection rates.
• 3- Shunt systems may over drain leading to
  subdural haemorrhage .
• 4- Other complications are seizures (5), CSF
  leak, stroke and intracerebral haemorrhage (lt 1).

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Brain Tumors

• More than 120 types
• Can occur in any part of the brain or Spinal
  Cord
• The Brain contains both Neurons and glial cells
• and is covered by the meninges and also
  contains blood vessels
• Brain Tumors
• Are classified according to the type of cell
  which causes the tumor.
• Can be fast or slow growing often different in
  children

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Primary Brain Tumors

• Start in the brain itself
• Often involve many types of tumor cells
• Most tumors come from Astrocytes
• When come from glial cells called gliomas
• Astrocytoma
• Anaplastic Astrocytoma
• Glioblastoma pendymona
• Oligodendroglioma
• Tumors in the Meninges
• Meningiomas
• Tumors in Nerves at the Base of the Brain
• Acoustic neuromas
• Schwannomas
• Pituitary gland

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Secondary Brain Tumors

• Tumors that come from outside the brain
  metastatic brain tumors
• Liver
• Breast
• Lung
• Resemble the cells where the tumor started.

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Symptoms of Brain Tumors

• A) Increased intracranial tension ( ?)
• B) Symptoms depend on the site of the tumor
  (Focal deficits)
• Frontal lobe muscle weakness, confusion.
• Temporal Lobe Seizures, aphasia.
• Occipital Lobe Visual disturbance .
• Parietal Lobe Loss of sensation.
• As becomes larger, more tissue is destroyed and
  tumors can also infiltrate ,makes it more
  difficult to be removed

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Investigation

• Plain X Ray skull
• CT scan
• MRI
• Carotid angiography

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Standard treatment

• Use a combination of
• Surgery
• Radiotherapy
• Chemotherapy

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Pituitary tumours

• The majority are benign adenomas .
• The most common pituitary adenomas are
• Prolactinoma (30),
• Non-functioning adenoma (20),
• Growth hormonesecreting adenoma (15)
• adrenocorticotrophic hormone (ACTH)-secreting
  adenoma (10).
• Clinical features
• Pituitary adenomas may present with mass effect
  or endocrine disturbance.
• Mass effect may cause a bitemporal hemianopia due
  to pressure on the optic chiasma or cause
  dysfunction of cranial nerves III, IV and VI .
• Endocrine dysfunction will depend on the
  secretory properties of the tumour if any
  galactorrhoea and primary/secondary amenorrhoea
  in a prolactinoma, Cushing syndrome in an
  ACTH-producing tumour (Cushings disease) and
  acromegaly or gigantism in a growth
  hormone-secreting tumour
• Pituitary apoplexy results in the sudden onset of
  headache, visual loss, ophthalmoplegia and
  possibly altered conscious level. It is caused by
  haemorrhagic infarction of a pituitary tumour.
  Preoperative resuscitation should include steroid
  cover, and urgent decompression is usually
  required.

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Investigation

• A patient with a suspected pituitary tumour
  should undergo formal
• Visual field and acuity testing.
• MRI scan of the pituitary region
• Baseline assessment of pituitary function
  including
• Prolactin,
• Fasting serum and urinary free cortisol,
• Growth hormone
• Insulin-like growth factor-1
• Follicle-stimulating hormone
• Luteinising hormone
• Thyroid function.

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Treatment

• The aim of treatment of pituitary tumours is to
  alleviate mass effect, restore or replace normal
  endocrine function and prevent recurrence.
• Prolactinomas should be initially treated
  medically with dopamine agonists such as
  cabergoline or bromocryptine.
• Growth hormone-secreting tumours may be amenable
  to medical treatment with somatostatin analogues
  such as octreotide or dopamine agonists.
• Surgical management of pituitary tumours requires
  transsphenoidal surgery either with an operating
  microscope or endoscope assisted.
• Large tumours with suprasellar extension may
  need to be managed by craniotomy as well
• Complications of trans-sphenoidal surgery include
  CSF leak , visual deterioration , major vessel
  injury and panhypopituitarism . Diabetes
  insipidus occurs following manipulation of the
  pituitary stalk and is usually transient.

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Vestibular Schwannoma (acoustic neuroma)

• Vestibular Schwannoma is the most common
  intracranial nerve sheath tumor and is benign. It
  may occur sporadically or in association with
  neurofibromatosis type 2 (bilateral vestibular
  Schwannomas being diagnostic of this condition).
• Presentation is usually with a combination of
  hearing loss, tinnitus
• and disequilibrium. Facial numbness and weakness
  are less common. Large tumours may present with
  symptoms of brainstem compression or
  hydrocephalus.
• Imaging with MRI will demonstrate the tumour .
• Differential diagnosis includes meningioma,
  metastasis and epidermoid tumor.
• Management depends on the size of the tumour and
  the presentation.
• Small intracanalicular tumours may be treated by
  radiological surveillance.
• Larger tumours could be considered for
  radiosurgery or craniotomy and excision.
• Hydrocephalus may need to be relieved via a
  ventriculoperitoneal shunt.
• Preservation of facial nerve and hearing function
  will depend on preoperative function as well as
  the size of the tumour.

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Brain Abscess
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Etiology

• Organism
• Streptococcus Klebsiella, Staphylococcus aureus,
  and anaerobes are also frequent.
• In immunocompromised patients, it is important to
  include Toxoplasma, and Nocardia as possible
  etiologic agents, as well as fungal pathogens.
• Source Classically, these abscesses arise
• Locally from otorhinolaryngeal infections like
  (Sinus, ear, or dental infections ) Or
• Hematogenously from distant infections. Or
• Head trauma blunt, penetrating, or surgical

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Clinical picture

• Headache, nausea, vomiting , blurring of vission
  , and altered mental status can occur due to
  increased intracranial pressure, while unilateral
  headache, seizures, and many focal neurological
  deficits occur due to the presence of a mass
  lesion. Fever and nuchal rigidity are also seen
  in many cases.
• Investigation
• The key to diagnosing brain abscess is
  correlating the clinical scenario with an imaging
  study, such as contrast-enhanced CT or MRI. The
  classic finding on CT or MRI is a circular lesion
  with a strongly contrast-enhancing surround rim.

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Treatment

• Treatment should also be aimed at correcting the
  primary source of infection .
• Initial surgical treatment usually consists of
  needle aspiration of the abscess. A total
  excision can be performed if the abscess is in
  its chronic, encapsulated form.
• Antibiotic therapy typically consists of 6 to 8
  weeks of intravenous treatment followed by 4 to 8
  weeks of oral treatment.
• Patients should receive routine follow-up imaging
  and should also be started on an antiepileptic
  medication.
• Glucocorticoids should be considered to
  counteract symptomatic intracranial hypertension.

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Trigeminal neuralgia
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Anatomy
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Introduction

• Neuralgia
• Unexplained peripheral nerve pain
• The most common site head and neck
• The most frequently diagnosed form trigeminal
  neuralgia (TN)
• Female predominance (male female 12)

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Characteristics of trigeminal neuralgia

• paroxysms of severe, lancinating , electric
  shock-like bouts of pain restricted to the
  distribution of the trigeminal nerve
• Unilaterally
• The mandibular and/or maxillary branch or,
  rarely, the ophthalmic branch
• Spontaneously attack or triggered by trigger zone
  movement of the face
• Seconds to minutes
• During an attack of TN, the sufferer will almost
  always remain still and refrain from speech or
  movement of the face, so as not to trigger
  further attacks of pain. The face may contort
  into a painful wince.

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Pathogenesis of trigeminal neuralgia

• Traumatic compression of the trigeminal nerve by
  neoplastic (cerebellopontine angle tumor) or
  vascular anomalies
• Infectious agents
• Human herpes simplex virus (HSV)
• Demyelinating conditions
• Multiple sclerosis (MS)

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Treatment

• Medical treatment
• Carbamazepine (Tegretol) first line
• Oxcarbazepine
• Gabapentin (Neurontin)
• Lamotrigine
• Baclofen
• Phenytoin
• Clonazepam
• Valproate
• Mexiletine
• Topiramate

Second line
Others
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• Surgical treatment
• Gasserian ganglion-level procedures
• Microvascular decompression (MVD)
• Ablative treatments
• Radiofrequency thermocoagulation (RFT)
• Balloon compression (BC)
• Stereotactic radiosurgery (SRS)
• Peripheral procedures
• Peripheral neurectomy
• Cryotherapy (cryonanlgesia)
• Alcohol block