Neurology II Flashcards

1
Q

Brainstem death

A

Brainstem death is regarded as the legal equivalent of death as customarily defined by cessation of heart beat and spontaneous respiration. In order to make the diagnosis of brain death, certain preconditions must be satisfied:

  • The patient’s condition must be known to be due to irreversible brain damage of known aetiology.
  • The patient must be in apnoeic coma, i.e. deeply unconscious and dependent on artificial ventilation.
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2
Q

Brainstem death exclusion criteria

A

There should be no doubt that other, potentially reversible, causes of the state of unconsciousness have been excluded, these include:

• Residual drug effects – effects of narcotics, hypnotics, tranquillisers and muscle relaxants

• Hypothermia – this must be excluded; the core
temperature must be 35degrees celsius

• Circulatory, metabolic and endocrine disturbances, e.g. hypernatraemia, diabetic coma.

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3
Q

Brainstem reflexes

A
  • Pupillary
  • Absent corneal reflexes
  • No motor response to central stimulation
  • Absent gag reflex
  • Absent cough reflex
  • Absent vestibulo-ocular reflex
  • Absence of spontaneous breathing
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4
Q

Brainstem reflexes: Pupillary

A

• Pupillary: There should be no pupillary response to light. The pupils do not respond either directly or consensually to sharp changes of the intensity of incident light. Cranial nerves involved in this reflex are II and III.

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5
Q

Brainstem reflexes: Corneal reflexes

A

• Absent corneal reflexes. There should be no response to direct stimulation of the cornea. This would normally result in blinking of the eye. The cranial nerves tested are V and VII.

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6
Q

Brainstem reflexes: Central stimulation

A

• No motor response to central stimulation. There should be no motor response within the cranial nerve distribution in response to adequate stimulation of any somatic area. The usual test is to apply supraorbital pressure.

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7
Q

Brainstem reflexes: Absent gag reflex

A

• Absent gag reflex. The back of the throat is touched with a catheter. There should be no gagging. This tests cranial nerves IX and X.

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8
Q

Brainstem reflexes: Cough reflex

A

• Absent cough reflex. There should be no response to bronchial stimulation by a catheter passed via the endotracheal tube. This tests cranial nerves IX and X.

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9
Q

Brainstem reflexes: vestibulo-ocular reflex

A

• Absent vestibulo-ocular reflex. There should be clear access to the tympanic membrane which is confirmed by visual inspection with an auriscope. The head is flexed at 30o. There should be no eye movements following slow injection of 50 mL of ice cold water over one min into each external auditory meatus in turn. This tests cranial nerves VIII, III and VI.

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10
Q

Spontaneous breathing

A

1) Finally, spontaneous respiration must be demonstrated to be absent despite a stimulus that should provoke it. Performed by disconnecting the patient from the ventilator in the presence of a PaCO2 above the threshold for respiratory stimulation. This is performed by preoxygenating the patient with 100% oxygen for at least ten min.
2) The PaCO2 is allowed to rise to 5.0 kPa before test- ing. The patient is then disconnected from the ventilator. Oxygen is insufflated at 6 L/min via an endotracheal tube to maintain adequate oxygenation during the test, and the PaCO2 is allowed to rise above 6.65 kPa.
3) There should be no spontaneous respirations noted. These tests should be carried out on two occasions, the time interval between the tests being a matter of clinical judgement. The tests should be carried out by two medical practitioners registered for more than five years, at least one of whom should be a consultant. They should be competent in the field and not members of the transplant team.

The legal time of death is on completion of the first set of brainstem tests, although death is not confirmed until the second set of tests is satisfied.

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11
Q

Head injury

A

Head injuries may be classified according to their aetiology, i.e. missile or non-missile (blunt) injuries. Missile injuries have been referred to as penetrating injuries in the past, but in some cases the missile does not penetrate but causes a depressed fracture without penetrating brain substance.

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12
Q

Head injury: missile injury

A

These may be divided into three types:

  • Depressed injury, where the missile causes a depressed fracture but does not enter the brain;
  • Penetrating injuries, where the missile enters the skull cavity but does not leave
  • Perforating injuries, where the missile enters and leaves the skull cavity. This type of injury is usually caused by high velocity bullet wounds, and the brain damage is extensive.
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13
Q

Head injury: Non-missile injury

A

These most commonly occur in road traffic accidents, falls and assaults. Damage may be minor or may result in severe injuries which are rapidly fatal. Brain damage occurs often as a result of acceleration/deceleration creating rotational and shearing forces which act on the mobile brain anchored within the rigid skull. Head injuries which may be fatal can occur without skull fractures.
Two main patterns of brain damage occur which are referred to as primary and secondary.

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14
Q

Primary brain damage

A

Contusions
These occur when the brain is crushed when coming into contact with the skull. They usually occur at the site of impact but may be severe on the side opposite the impact, i.e. contre-coup lesions.

Large contusions may be associated with intracerebral haemorrhage.

Diffuse axonal injury This occurs as a result of acceleration/deceleration and rotational move- ments. It may occur in the absence of a skull fracture. The majority of changes are usually only detectable on histology. Patients who have sustained diffuse axonal injury and survive are usually severely disabled.

Treatment cannot reverse primary brain injury. It is aimed at prevention, recognition and treatment of secondary brain damage.

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15
Q

Secondary brain damage

A

This occurs as a result of complications developing after the time of injury. Secondary brain damage may result from:

  • intracranial haemorrhage
  • cerebral hypoxia
  • cerebral oedema
  • intracranial herniation
  • infection
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16
Q

Sequelae of head injuries

A

Most patients make a satisfactory recovery unless the head injury is severe, when up to 10% may be severely disabled. Consequences of severe head injuries include:
• Death (often diagnosed as brainstem death)
• Persistent vegetative state;
• Post-traumatic epilepsy;
• Traumatic hemiplegia;
• Post-traumatic dementia
• Cranial nerve palsies.

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17
Q

Intracranial haemorrhage

A

This is usually an expansile haematoma within brain tissue. Most arise in hypertensive patients who have weak spots (microaneurysms) on their arteriosclerotic cerebral vessels.

Other causes include

1) Bleeding into a tumour
2) Vascular malformations
3) Bleeding associated with coagulopathies

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18
Q

Extracerebral haemorrhage

A

These are divided into different types according to where they occur in relationship to the meninges. Extradural and subdural haemorrhages usually occur following trauma. Subarachnoid haemorrhage usually occurs following rupture of a ‘berry’ aneurysm and may also occur following trauma.

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19
Q

Extradural haemorrhage

A

This is bleeding into the extradural space between the skull and dura. It is caused by a head injury, usually with a skull fracture which causes tearing of an artery or a venous sinus.

Classically the injury is to the middle meningeal artery following fracture of the temporal bone. The haematoma lies outside the dura and causes compression of the underlying brain as it expands.

Clinically there is usually a lucid interval followed by a rapid increase in intracranial pressure.

Transtentorial herniation may occur and manifest itself by reduction in conscious level and by brainstem compression. The condition is fatal unless diagnosed early and treated surgically by evacuation of the clot.

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20
Q

Subdural haemorrhage

A

This is bleeding into the subdural space between the dura and arachnoid mater. Bleeding is usually from small ‘bridging’ veins which cross the subdural space. Trauma is the usual cause. Two types are described as follows.

Acute subdural haematoma This is commonly seen following head injury, often associated with a lacer- ated brain resulting from high speed injuries. The haematoma spreads over a large area. The patient usually has marked brain injury from the outset and is comatose, but the condition deteriorates further.

Chronic subdural haematoma This is usually seen in the elderly. Brain shrinkage makes the ‘bridging’ veins between cerebral cortex and venous sinuses more vulnerable. It may result from a trivial and forgotten head injury. It may occur weeks or months after the injury. Presentation is with personality change, memory loss, confusion, and fluctuating level of consciousness.

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21
Q

Subarachnoid haemorrhage

A

This is bleeding into the subarachnoid space between the arachnoid and pia mater. Causes include:
• trauma in association with head injury;
• rupture of a ‘berry’ aneurysm;
• rupture of a vascular malformation;
• hypertensive haemorrhage;
• coagulation disorders;
• rupture of an intracerebral haematoma into the
subarachnoid space;
• tumours; and
• vasculitis.

Subarachnoid haemorrhage presents with sudden onset of severe headache. Blood spreads over the cerebral surface of the subarachnoid space. In approximately 15% of cases it is instantly fatal, a further 45% of cases dying later due to rebleeding.

Blood accumulates in the basal cisterns and may block the egress of CSF, caus- ing hydrocephalus. This can occur early or later in survivors where fibrous obliteration of the subarachnoid space occurs due to organisation of the clot.

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22
Q

Space occupying lesions

A

These may result from a variety of causes. They cause an expansion in volume of the cranial contents and will eventually cause raised intracranial pressure.

Intracranial space-occupying lesions may be either diffuse or focal. Diffuse brain swelling results from either vasodilatation or oedema.

Focal brain swellings include tumours, abscess and haematomas. The consequences of intracranial space-occupying lesions include:
• Raised intracranial pressure
• Intracranial shift
• intracranial herniation 
• hydrocephalus
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23
Q

Raised intracranial pressure

A

The skull is a rigid container in which brain, CSF and blood are the only contents. At normal intracranial pressures (10–15 mmHg or 12–18 cmH2O), these three components are in volumetric equilibrium, i.e. ICP =CSF + Brain + Blood. This formula is the basis for the Monro-Kellie hypothesis which states that the ICP will increase if the volume of one component is increased. The increase in ICP can only be compensated for by a decrease in one or both of the other components. The compensatory properties among the intracranial con- tents follow a pressure/volume exponential curve.
Increased volume of any of the three components can be balanced up to a certain level without any increase in the intracranial pressure. However, eventually a critical volume is reached when any further vol- ume increase results in raised intracranial pressure.

The effects of raised intracranial pressure are:
• hydrocephalus;
• cerebral ischaemia;
• brain shift and herniation
• systemic effects.
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24
Q

Raised intracranial pressure: hydrocephalus

A

This is a common complication of space-occupying lesions where an increase in ICP may result in the interruption of CSF flow. This is most commonly seen in lesions of the posterior cranial fossa which compress the cerebral aqueduct and fourth ventricle.

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25
Q

Raised intracranial pressure: Cerebral ischaemia

A

The effects of raised intracranial pressure are exerted on the vascular component and result in progressive reduction in cerebral perfusion pressure. (Cerebral perfusion pressure = blood pressure – intracranial pressure.)

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26
Q

Brainshift and herniation

A

These usually occur following a critical increase in intra- cranial pressure. Lumbar puncture is contraindicated in any patient with raised intracranial pressure, as there is a risk of precipitating a potentially fatal brainstem herniation. Herniations occur at some specific sites:

Transtentorial herniation

Tonsillar herniation

Subfalcial herniation

Diencephalic herniation

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27
Q

Transtentorial herniation

A

Transtentorial herniation
A laterally placed supra- tentorial mass may push the uncus and hippocampus over the tentorium cerebelli. The oculomotor nerves, cerebral peduncles, cerebral aqueduct, posterior cerebral artery, and brainstem may be compressed by the displaced temporal lobe. Transtentorial herniation is
frequently fatal because of the secondary haemorrhage into the brainstem.

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28
Q

Tonsillar herniation

A

Tonsillar herniation Herniation of the cerebellar tonsils into the foramen magnum causes compres- sion of the medulla. Medullary compression results in decerebrate posture, respiratory failure, and subsequent death.

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29
Q

Subfalcial herniation

A

Subfalcial This is caused by a lesion in one hemi- sphere and leads to the herniation of the cingulate gyrus under the falx cerebri.

30
Q

Diencephalic herniation

A

Diencephalic Generalised brain swelling leads to the midbrain herniating through the tentorium. This is termed ‘coning’.

31
Q

Clinical manifestations of tentorial herniation

A

1) Oculomotor nerve (Cranial III) = Ipsilateral pupillary dilatation
2) Ipsilateral cerebral peduncle = Contralateral hemiparesis
3) Contralateral cerebral peduncle = ipsilateral hemiparesis
4) Posterior cerebral artery = Cortical blindness
5) Cerebral aqueduct = Headache and vomiting from hydrocephalus
6) Reticular formation = Coma
7) Midbrain = Decerebrate rigidity, death

32
Q

Systemic effects

A

Systemic effects of raised intracranial pressure are thought to result from autonomic imbalance and over- activity as a result of compression of the hypothalamus. They include:

  • hypertension
  • bradycardia
  • respiratory slowing
  • pulmonary oedema (often haemorrhagic)
  • gastrointestinal ulceration (Cushing’s ulcer)
33
Q

Clinical manifestations of raised intracranial pressure

A

Once the phase of compensation between the three components, i.e. brain, CSF and blood, is passed, further increase in volume of intracranial contents will cause an increase in intracranial pressure. The clinical signs and symptoms are:

  • Headache – due to distortion and compression of pain receptors within the dura mater and around cerebral blood vessels
  • Nausea and vomiting – due to pressure on the vomiting centre in the pons and medulla
  • Papilloedema due to venous obstruction

• Decrease in level of consciousness ranging from drowsiness to coma depending on the degree of
raised intracranial pressure.

34
Q

Meningitis

A

Bacterial meningitis is the only form of meningitis which the surgical trainee is likely to encounter. Bacteria gain access to the CNS by four main routes:

  • Direct spread from an adjacent focus of infection, e.g. middle ear, mastoid, paranasal sinuses, osteomyelitis of vertebrae or skull
  • Blood-borne as part of septicaemia or septic embolus from bacterial endocarditis or bronchiectasis
  • Penetrating wounds, including skull fractures

• Iatrogenic, e.g. following lumbar puncture or spinal anaesthesia or following neurosurgical
procedures.

Meningitis may affect predominantly the dura mater (pachymeningitis) or the arachnoid or pia mater (lep tomeningitis). The latter is the more common.

35
Q

Pachymeningitis

A

This is usually a consequence of direct spread of infection following otitis media or mastoiditis and is a complication of skull fractures.

Common pathogens include haemolytic streptococci from the paranasal sinuses, or Staph. aureus from skull fractures.

Epidural abscess (pus between skull and dura mater) or subdural abscesses (pus in the subdural space) may result.

36
Q

Leptomeningitis

A

This is usually a result of blood-borne spread of infection or may arise from direct spread from the skull bones. Different organisms cause infection at different ages:
• Neonates – E. coli, Salmonella
• Children – H. influenzae type b, Neisseria
meningitidis, Streptococcus pneumoniae
• Adults – Neisseria meningitidis, Streptococcus pneumoniae
• Elderly – Listeria monocytogenes, Streptococcus pneumoniae.

Meningococcal meningitis is the commonest variety. The organism is spread by droplets from asymptomatic nasal carriers. The organism reaches the CNS by hae- matogenous spread. Onset of the illness is rapid with a petechial rash related to disseminated intravascular coagulation, accompanied by adrenal haemorrhage (Waterhouse–Friderichsen syndrome) which is often fatal.

37
Q

Complications of bacterial meningitis

A
Complications of bacterial meningitis include:
• Cerebral infarction
• Cerebral abscess
• Subdural abscess
• Hydrocephalus
• Epilepsy
38
Q

Cerebral abscess

A

Cerebral abscesses usually develop following focal inflammation of the parenchyma of the brain. They usually occur as a result of:

  • direct spread of infection from sepsis in the middle ear or paranasal sinuses;
  • septic cerebral sinus thrombosis due to spread of infection from the mastoid or middle ear via the sigmoid sinus;
  • blood-borne infection, e.g. from infective endocarditis or bronchiectasis. In immunocompromised patients, abscesses may be caused by fungal or protozoal organisms; and

• trauma – following open skull fractures.
Abscesses may occur in preferential sites according to their aetiology:

  • temporal lobe or cerebellum from otitis media; • frontal lobe from paranasal sinuses; and
  • parietal lobe from haematogenous spread.
39
Q

Complications of cerebral abscess

A
Complications of cerebral abscesses include:
• meningitis
• intracranial herniation
• focal neurological deficit
• epilepsy

Cerebral abscesses often cause a dramatic increase in intracranial pressure because of massive surrounding oedema. Lumbar puncture should not be performed in the presence of cerebral abscess, as this may precipitate fatal intracranial herniation.

40
Q

Cells of the CNS

A
The constituent cells of the nervous system can be divided into five main groups:
• neurons
• glia
• microglial cells
• connective tissue
• blood vessels.

Glial cells are specialised supporting cells of the CNS and comprise four main cells:

1) Astrocytes
2) Oligodendrocytes
3) Ependymal cells
4) Choroid plexus cells. Micro- glial cells belong to the macrophage/monocyte system of phagocytic cells.

They are important in reactive states, for example in inflammation and demyelinating disorders. The connective tissue in the central nervous system is confined to two main types, i.e. the meninges and perivascular fibroblasts.

41
Q

Cerebral tumours classification

A
Primary
• Glial (gliomas) 
Astrocytomas
Medullablastomas 
Ependymomas 
Oligodendrogliomas

• Non-glial
Meningiomas
Acoustic neuromas
Pituitary tumours

• Secondary
Lung 
Breast 
Kidney 
Melanoma
42
Q

Cerebral tumours

A

Cerebral tumours may be broadly classified into two types; glial and non-glial, depending on their cell of origin disease.

Acoustic neuroma should always be considered in a patient with unilateral sensorineural deafness with tinnitus. It usually occurs in the age range 30–60.

Facial weakness with unilateral taste loss is a later manifestation. The corneal reflexes are lost relatively early when the trigeminal nerve is stretched by the tumour.

Dysphagia, hoarseness and dysarthria may arise due to involvement of nerves IX, X and XI.

Unilateral cerebellar signs and features of raised ICP may occur, but these are now a rare occurrence.

43
Q

Secondary tumours

A

The commonest neoplasms to metasasize to the CNS are carcinoma of the breast, bronchus, kidney, colon, and also malignant melanomas.

44
Q

Clinical features of CNS tumours

A

CNS tumours may present clinically in two main ways:
• local effects – these may include cranial nerve palsies, epilepsy, or paraplegia with a spinal cord tumour

• mass effects – many tumours may present with non-specific signs of space-occupying lesions without any localising signs. These symptoms include confusion, drowsiness, headache and vomiting. Other features may relate to the development of hydrocephalus and intracranial herniation.

45
Q

Pituitary tumours

A

These cause symptoms because of their endocrine capacity or their effects on the optic chiasma.

Secretory tumours (e.g. prolactinoma) 
Many tumours contain a mixture of secretory cells. Presentation is influenced by the hormonal production and the size of the tumour. Secretory tumours are usually small.

Non-secretory tumours
These usually grow to a large size and present through local effects. The symptoms and signs depend upon whether they arise from the endocrine capacity or local pressure effects. Bitemporal hemianopia results from compression of the optic chiasma. Compression of secretory cells by non-secretory tumours may result in hypopituitarism. Symptoms include reduced libido, infertility, amenor- rhoea, myxoedema, depression, loss of sex character- istics, and hypoadrenalism. In children, growth arrest
may occur. Hormonally active tumours may result in the following:
• overproduction of growth hormone: before fusion of the epiphyses, this will cause gigantism; in adult life acromegaly results;
• hyperprolactinaemia: this is characterised by amenorrhoea, infertility, galactorrhoea, and impotence; and
• Cushing’s disease

46
Q

Spinal Cord injuries/compression

See diagram on anatomy

A

Cord injuries
Over 80% of spinal injuries result from road traffic accidents, the remainder resulting from falls and other trauma, e.g. penetrating wounds. Penetrating trauma may result in incomplete cord transection which may manifest clinically as Brown–Séquard syndrome (see below).

Closed injuries are responsible for most spinal cord trauma and are usually associated with fractures or fracture/dislocations of the vertebral column. As with brain injuries there is primary and secondary damage:

  • Primary damage – contusions, transections, haemorrhage, necrosis; and
  • Secondary damage – extradural haematoma, infarction, infection, oedema.

Contusion or laceration is the usual result of spinal cord injury. There is resulting oedema and increased tissue pressure, and this, together with cord haemor- rhage, further limits the blood supply. The distribution of cord oedema, of haemorrhage and of infarction determines the neurological symptoms and the signs elicited at the time of evaluation. Spinal cord injuries may be complete or incomplete.

47
Q

Complete spinal cord injury

A

When the spinal cord is transected there are three major and immediate effects:

  • Loss of voluntary movement in all parts innervated by the isolated spinal segment, i.e. distal to the level of transection; this loss is irreversible;
  • A loss of all sensation from those areas which depend on ascending spinal pathways crossing the site of injury

• Spinal shock.
With complete cord transection there is no voluntary nervous function below the injury site. There is an initial phase of spinal shock with a loss of all reflexes below the injured cord. These include the bulbocavernosus and anal reflexes, and deep tendon reflexes. Spinal shock may last for a few hours to several weeks. The cessation of the spinal shock phase is marked by return of reflex activity in the spinal cord when the lesion is above the sacral segment, i.e. when there is an upper motor neuron lesion. The anal and bulbocavernosus reflexes are usually the first to return. The anal and bulbocavernosus reflexes both depend on intact sacral reflex arcs. The anal reflex is elicited by pricking the perianal skin with a pin when there is a visible contraction of the anal sphincter. The bulbocavernosus reflex is contraction of the anal sphincter in response to squeezing the glans penis.

48
Q

Incomplete spinal cord injury

A

In incomplete spinal cord injuries some function is present below the site of the injury. These injuries have a more favourable prognosis overall. There are recognised patterns of incomplete cord injury, although these are rarely ‘pure’ and variations may occur. The functional anatomy of the tract of the spinal cord has already been described. The dorsal columns contain fibres serving fine and discriminative tactile sensation as well as proprioception.

The lateral corticospinal tract (crossed pyramidal tract) controls skilled vol- untary movement, and the fibres in these tracts are somatopically arranged, fibres for the lower part of the cord being lateral and those for the upper levels medial.

The spinothalamic tracts conduct pain and temperature sensation. Pain and temperature fibres enter the posterior roots, ascend a few segments, relay in the substantia gelatinosa, then cross to the opposite site to ascend in these tracts to the thalamus, where they are then relayed to the sensory cortex. The fibres in these tracts are somatotopically arranged, those for the lower limb being superficial and those for the upper limb deepest in the cord.

49
Q

Anterior cord syndrome

A

Anterior cord syndrome Damage to the anterior cord is particularly associated with flexion/rotation injuries to the spine, producing an anterior disloca- tion or by compression fracture of a vertebral body with bone encroaching on the vertebral canal. In add- ition to direct damage there is often compression of the anterior spinal artery so that the corticospinal and spinothalamic tracts are damaged by a combination of direct trauma and ischaemia. The result of this lesion is a loss of power as well as reduction of pain and temperature sensation below the lesion. Since the dorsal columns remain intact, touch and proprioception are unaffected.

50
Q

Central cord syndrome

A

This is typically seen in the older patient with cervical spondylosis who sustains a hyperextension injury. This may be from relatively minor trauma. The spinal cord is compressed between the osteophytes of the vertebrae and intravertebral disc in front and the thickened ligamentum flavum posteriorly. The more centrally situated cervical tracts supplying the arm tend to be more involved than the more peripherally placed tracts affecting the legs. Classically there is a flaccid (lower motor neu- ron) weakness of the arms but, because the distal leg and sacral motor and sensory fibres are located most peripherally in the cervical cord, perianal sensation and some lower extremity movement and sensation may be preserved.

51
Q

Posterior cord syndrome

A

This syndrome is most commonly seen in hyperextension injuries with frac- tures of the posterior elements of the vertebrae. The posterior columns are involved and, therefore, pro- prioception is affected. The patient usually has good power and sensation for pain and temperature below the lesion, but there may be profound ataxia due to the loss of proprioception which produces an unsteady and faltering gait.

52
Q

Brown–Séquard syndrome

A

This is hemisection of the cord. It may result from either stab injuries or fractures of the lateral mass of the vertebrae. The classical picture is paralysis on the affected side below the lesion (pyramidal tract), and also loss of prop- rioception and fine discrimination (dorsal columns). Pain and temperature are normal on the side of the lesion but are lost on the opposite side below the lesion because the affected spinothalamic tract carries fibres which have decussated below the level of cord hemisection. The uninjured side, therefore, has good power but reduced or absent sensation to pin prick and temperature.

53
Q

Cauda equina syndrome

A

This syndrome may arise from bony compression or disc protrusions in the lumbar or sacral region, with compression of the lumbosacral nerve roots below the conus medullaris.

This is a lower motor neuron lesion, and bowel and bladder dysfunction, as well as leg numbness and weakness, occur commonly with this syndrome.

54
Q

Autonomic defects in spinal cord injuries

A
Vasomotor control 
Temperature control 
Bladder control 
Spinal shock
UMN
LMN
Bowel
Autonomic dysreflexia
55
Q

Autonomic defects in spinal cord injuries: Vasomotor control

A

Vasomotor control
Problems with hypotension arise in cervical or high thoracic lesions, i.e. those above the sympathetic outflow (T5). Because of interruption of sympathetic splanchnic control, the upright position results in hypotension secondary to impaired venous return, with consequent syncope. Adaptive mechanisms possibly related to spinal reflexes occur with time. Control of the vasomotor system is labile during the first few days after a cervical spinal cord injury. There is a risk of sudden cardiac arrest following turning of the patient.

56
Q

Autonomic defects in spinal cord injuries: Temperature control

A

Temperature control
The patient does not have the usual thermoregulatory mechanisms working below
the level of the lesion. This is particularly so in quadriplegics. The mechanisms allowing for vasoconstriction to conserve heat are lost. The patient is unable to shiver and consequently is unable to increase the body temperature. Also, the patient cannot sweat below the level of the lesion in response to hyperthermia. The quadriplegic patient, therefore, tends to assume the tempera- ture of the environment.

57
Q

Autonomic defects in spinal cord injuries: Bladder control

A

Bladder control
After a spinal injury the effect on the bladder depends on the level of injury, degree of damage, and the time interval after the injury.

58
Q

Autonomic defects in spinal cord injuries: Spinal shock

A

• Spinal shock. There is flaccid paralysis below the level of the lesion with absent reflexes. The patient develops acute retention of urine and requires catheterisation.

59
Q

Autonomic defects in spinal cord injuries: UMN

A

• Upper motor neuron lesion. If this is above the sacral segments, reflex activity returns after the phase of spinal shock passes and an automatic type of bladder results, i.e. the bladder empties involuntarily as it fills with urine. There is no sensation of bladder fullness.

60
Q

Autonomic defects in spinal cord injuries: LMN

A

• Lower motor neuron lesion. The reflex arc is interrupted and an autonomous bladder results. Bladder function is governed by a myogenic stretch reflex inherent in the detrusor muscle. There is a linear increase in intravesical pressure with filling until capacity is reached. Overflow incontinence then occurs.

61
Q

Autonomic defects in spinal cord injuries: Bowel

A

Mixed types of lesions may occur with damage to the conus medullaris and cauda equina.
Bowel In a spinal cord lesion above the sacral seg- ments the defaecation reflex is intact but automatic emptying of the lower bowel will occur because the normal control exercised by voluntary contraction of the external sphincter is lost and sensation is impaired. The external sphincter will be hypertonic in an upper motor neuron lesion. In a lower motor neuron lesion the reflex is interrupted but the autonomous bowel has intrinsic contractile mechanisms. The external anal sphincter is weak, and the anus is patulous with absent tone.

62
Q

Autonomic defects in spinal cord injuries: Autonomic dysreflexia

A

This is seen in patients with cervical cord injuries above the sympathetic outflow but may also occur with high thoracic lesions above T5. It occurs after the period of spinal shock has worn off and results from distension of the bladder, which causes reflex sympathetic overactivity below the level of the spinal cord lesion, causing vasoconstriction and systemic hypertension. The carotid and aortic baroreceptors are stimulated and respond via the vasomotor centre with increased vagal tone, with resultant bradycardia.

The peripheral vasodilatation which would have normally relieved the hypertension does not occur because the stimuli cannot pass dis- tally through the severed cord. The patient develops a severe headache with profuse sweating and flushing of the skin above the level of the lesion. Intracranial haemorrhage may occur.

63
Q

Spinal cord and nerve root compression

A
The following are the main causes of spinal cord and nerve root compression:
• prolapsed intravertebral disc;
• trauma;
• tumour, e.g. metastases, myeloma;
• infection, e.g. tuberculosis, abscess;
• skeletal disorders, e.g. osteoarthritis, Paget’s
disease; and
• vascular, e.g. haemorrhage, vascular
malformation.
64
Q

Prolapsed intravertebral disc

A

This usually occurs in the middle-aged or elderly due to degenerative disc disease but may occur in young adults following strenuous exercise. The posterior part of the annulus fibrosus is relatively thin. A tear occurs in the annulus fibrosus, and the gelatinous nucleus pulposus herniates out either posteriorly and poste- rolaterally. In the latter case it impinges on the nerve roots causing sciatica if it occurs in the lumbosacral region. Central herniation is less common but may cause direct cord damage and may occasionally com- press the anterior spinal artery, leading to infarction.

The commonest sites for disc prolapse are
L4/5
L5/ S1 or in the neck, C5/6 or C6/7

A prolapsed L4/5 disc produces pressure on the root of L5 nerve and that of L5/S1 on S1 nerve. Pain is referred to the back of the leg and foot along the distribution of the sciatic nerve (sciatica). With an L5 lesion there may be weakness of ankle dorsiflexion and numbness over the lower and lateral part of the leg and medial side of the foot. With an S1 lesion there will be numbness over the lateral side of the foot and the ankle jerk may be diminished or absent. Direct posterior pro- lapse of the disc may compress the cauda equina.

In the cervical region, prolapse occurs immediately above or below the 6th certvical vertebra so that the nerve roots affected are C6 or C7. Sensation may be diminished, especially in the thumb and index finger (C6) or middle finger (C7). Motor weakness may occur in triceps and the wrist dorsiflexors. The triceps jerk is sometimes reduced but usually the tendon reflexes are normal.

65
Q

Osteoarthritis

A

Spondylosis occurs due to osteoarthritis. It becomes progressively more common over the age of 40 and is often accompanied by degenerative disc disease. Osteophytes occur at the upper and lower margins of the vertebral bodies, adjacent to the attachment of the annulus fibrosus. The osteophytes encroach on the spinal canal or intravertebral foramina and irritate the nerve roots.

66
Q

Peripheral nerve lesions

A

Peripheral nerves contain sensory and motor axons (or both), most of which are myelinated. Each axon is surrounded by the endoneurium, a sheath of col- lagen fibres. Groups of axons, called fasciculi, are fur- ther surrounded by a connective tissue sheath called the perineurium. The fasciculi themselves are further surrounded by the epineurium, which is a thicker layer of connective tissue.

Nerve injury may be caused by one of the following:
• laceration
• contusion
• stretch 
• compression

Nerve injuries may be further classified according to the degree of damage:
• neuropraxia
• axonotmesis
• neurotmesis

67
Q

Neuropraxia

A

This results in temporary failure of conduction with- out loss of axonal continuity. Recovery is rapid and complete and takes a few days to a few weeks.

68
Q

Axonotmesis

A

This is complete division of an axon. If the axon is transected, that part of the axon no longer in continuity with the cell body dies (Wallerian degeneration). The axon distal to the site of injury degenerates. In myelinated fibres this is accompanied by breakdown of myelin around the degenerating axons. Degeneration commences at 3–4 days following injury. In axonotmesis the endoneurial tube remains intact and axonal regeneration can occur unless it is impeded by scar tis- sue at the site of injury (neuroma in continuity).

69
Q

Neurotmesis

A

This would occur in a nerve laceration. There is complete break in the nerve fibres, i.e. axon, myelin sheath, and endoneurial tube. When a peripheral nerve is severed the distal nerve degenerates. The axon then regenerates from the nerve cell through the rejoined sheaths. The rate of the repair is approximately 1 mm/ day. Unfortunately, individual nerves do not regenerate down their original nerve sheath, and motor axons may regenerate into a sensory distal sheath and vice versa. The functional results are, therefore, variable. The best results occur if the nerve is purely motor or purely sensory or in nerves rejoined by microscopical surgical techniques.

70
Q

UMN and LMN

A

Upper motor neurons commence in the motor cor- tex. Groups of cells control movements rather than individual muscles. The upper motor neurons synapse with the anterior horn cells in the spinal cord.

The lower motor neurons are from the anterior horn cells and end involuntary muscle. Lesions of anterior horn cells and ventral nerve roots will be entirely motor. Lesions of peripheral nerves will be mixed motor and sensory. Lower motor neurons are influenced by upper motor neurons and by the extrapyramidal system and modifications of muscle tone and reflexes result, when correct balance between the two neuron groups is lost.

71
Q

UMN vs LMN

A
Upper
Paralysis affects movements rather than muscle
Wasting slight
Muscles hypertonic (clasp-
knife rigidity) Tendon reflexes
increased
No trophic skin changes
Lower
Individual or groups of muscles affected Wasting pronounced
Muscles hypotonic (flaccidity)
Tendon reflexes absent or diminished
Skin often cold, blue and shiny

Upper reflexes
Superficial reflexes diminished:
– absentabdominalreflexes – Babinski sign present
(both are corticospinal reflexes in which the afferent arc is via a small number of ascending fibres in the corticospinal tracts)

Lower reflexes
Superficial reflexes unaltered unless sensationalsolost