Neurological Pathologies Flashcards
Increase in Intercranial Pressure
Aetiology
- Tumour masses
- Cerebral oedema
- Increase in volume of CSF
- Increase production
- Obstructed flow
- Reduced absorption
- Haemorrhage
- Craniosyntosis
- Cerebral venous thrombosis
- Increase in intracranial venous pressure
Clinical Features
- Change in the level of consciousness (confusion, drowsiness, eventually coma)
- Increase in arterial blood pressure
- Decrease in heart rate
- Alterations in respiration eg hyperventilation, Cheyne-Stokes respiration
- Nausea and vomiting
- Headache
- Pupils become dilated, and do not respond to light (due to CN 111 damage, as midbrain herniates and compresses nerves)
Compensatory Mechanism for Rasied ICP
- CSF displaced out of cranial vault, via increasing its reabsorption
- Reduction of blood volume by vasoconstriction and compression of intracranial veins
- Oxygenation of brain compromised, so systemic blood pressure elevates (due to systemic vasoconstriction), in an attempt to reduce the ICP
- Once the ICP reaches approximately 25 mmHg, any increase in intracranial content will cause a significant increase in the pressure.
Condequences of increased ICP
- Distortions and dislocations of brain substance. (herniation)
- Vascular damage: Papilloedema = oedema of optic disc (due to compression of central retinal v.), and hemorrhage or infarction in brain due to stretching and compression of blood vessels.
- Intracranial nerve damage, especially CNIII and VI.
- Obstruction to flow of CSF. § Changes in skull bones.
- Reduction of cerebral blood flow and perfusion pressure, causing more ischaemia
Cerebral Edema
3 types of mechanisms involved:
- Vasogenic
- Cytotoxic
- Interstitial
One or more of these mechanisms may be involved in a patient with cerebral oedema
Cerebral Herniation
Herniation refers to the abnormal movement of tissue through an opening (either normal or pathological)
Uncal herniation:
- Uncus (medial projection of temporal lobe) herniates under tentorium cerebelli
Central herniation:
- The diencephalon and parts of both temporal lobes
Cerebellar tonsillar herniation:
- Cerebellar tonsils herniate into foramen magnum
Cingulate herniation
- Cingulate gyrus herniates under falx cerebri
- Anterior cerebral artery may be compressed, resulting in infarction in area of distribution
- Clinical features would include sensory loss and weakness of contralateral leg and foot
Transcalvarial herniation
- Possible result of cerebral oedema occurring postsurgically, or following trauma
- There is herniation of part of the brain through a defect in the skull (either surgically created or from trauma)
Clinical Features
- Headache, nausea, vomiting, hypertension, reduced pulse rate (all non-specific features of raised ICP)
- Irregular breathing, altered consciousness, loss of pupillary light reflex (brainstem comp)
Alzhiemer’s Disease
- A degenerative process characterised by cortical atrophy and loss of neurons
- Predilection for the frontal and temporal lobes
- It accounts for 50-70% of dementias
Pathology
There is a degneration of the cerberum with lose of neurons and synapes. There is deposition of the proteins in the brian called plaques.
Clinical Features
- nsidious onset
- Memory loss (short term initially, later long-term memory loss)
- Confusion and disorientation
- Higher order functions affected - problem solving, judgement, abstract thinking
- Behavioural changes eg irritability, restlessness
- Mood changes
- Motor changes may occur as well
- Earlier onset usually associated with more rapid progression
Parkinson’s Disease
- Parkinsons Disease is a chronic degenerative disorder of basal ganglia involving cell death within the substantia nigra, leading to a decrease in dopamine.
- This results in variable combinations of slowness of movement (bradykinesia), rigidity, tremor and postural instability.
- It is the most common basal ganglia disease.
- It needs to be differentiated from ‘Parkinsonism’ (other disorders that cause a presentation of parkinson’s symptoms)
Clinical Features
- Begins insidiously with slowness of movement, weakness, and tremor.
- Tremor: Usually occurs at rest and disappears with movement, enhanced by emotional tension or fatigue, involves rhythmic movement of the thumb towards the fingers known as ‘pill rolling’.
- Micrographia
- Muscular aches, sensation of fatigue, and the face becomes mask like and open mouthed, with diminished blinking.
- The posture becomes stooped. They have difficulty in walking, where they shuffle with short steps and the arms are held flexed to the waist and fail to swing with the stride.
- Festination
- Poor balance - tendency to fall.
- Impairment of fine movements such as button fastening.
- Increased salivation.
- Increased muscle tone. This makes them stiff, causing difficulty in initiating voluntary movements. Very difficult to move in passive Range of Motion
- Characteristic mask expression
- At later stages of Parkinson’s disease, some dementia may be observed
Huntington’s Disease
- Huntington’s Disease is a chronic degenerative disorder of basal ganglia and parts of the cortex.
- There is striatum neuronal death, and cortical neuronal death. This leads to a decrease in ACh and GABA.
- In contrast to Parkinson’s, Huntington’s disease is classically associated with irregular, jerky and uncontrolled movements
Clinical Features
- Begins insidiously with subtle changes in behaviour and cognition.
- Next comes the hallmark feature of jerky, random and uncontrolled movements called chorea
- As it is an upper motor neuron condition, this is accompanied by muscle rigidity
- Then progresses to having difficulty with balance, eating, speaking and sleep
Amyotrophic Lateral Sclerosis
- A progressive degenerative disorder of upper and lower motor neurons within the CNS
- Is the most common form of motor neuron disease (MND)
- Characterised by progressive weakening and muscle atrophy, fasciculations, hypertonicity and hyperreflexia
Clinical Fetures
- Weakness
- Muscle wasting / atrophy
- Fasciculations
- Spasticity / hypertonicity
- Hyper-reflexia
- Difficulty with speech and/or swallowing
- Eventual incontinence
Acute Supperative Meningitis
Inflammation of the meninges of brain and/or spinal cord
Types
- Acute Bacterial Meningitis (common)
- Aseptic Meningitis (common)
- Sub-acute Meningitis
- Chronic Meningitis
Clinical Features
- A prodromal respiratory illness or sore throat often precedes the fever (pyrogens from microorganism)
- Headache (due to distended blood vessels and meningeal irritation).
- Pus will collect in occipital area due to gravity à generalised but more intense pain.
- Minor mechanical stimuli will increase the pain.
- Stiff neck: passive flexion of neck
- Brudzinski’s sign and Kernigs sign
- Nausea, vomiting
- Photophobia
- Specific symptoms related to the organism eg. purpuric rash in meningococcal infection
- Raised ICP
- Raised BP, reduced HR.
- Alterations to breathing
- Seizures and cranial neuropathies may be present
- Alteration to consciousness
- Dehydration and vascular collapse is common leading to shock
- Death
Infants or young children between 3 months and 2 years of age with an increasing irritability, poor feeding, vomiting, lethargy, seizures or signs of meningeal irritation, should be investigated for meningitis.
Aspeptic Meningitis
Meningeal inflammation from causes other than bacterial
- Similar to those of acute bacterial meningitis
- Mortality rate varies with aetiology
Encaphalitis
An acute inflammatory disease of the brain due to direct viral invasion or to hypersensitivity initiated by a virus or other foreign protein
Aetiology
Primary
- Viral (eg. echovirus, coxsackie virus, arbovirus, herpes simplex, varicella zoster, mumps). This may occur sporadically or in epidemics.
Secondary
- This is usually an immunological reaction to a viral infection eg. to measles, rubella, chicken pox.
Clinical Features
- Malaise and fever
- Symptoms and signs of meningitis
- Cerebral dysfunction - eg. alteration in consciousness, personality changes, seizures, paresis, cranial nerve abnormalities
Myelitis
Myelitis is inflammation of the spinal cord which can disrupt the normal responses from the brain to the rest of the body, and from the rest of the body to the brain. Inflammation in the spinal cord, can cause the myelin and axon to be damaged resulting in symptoms such as paralysis and sensory loss.
Spongiform encephalopathies
Rare. Transmissible spongiform encephalopathies (TSEs) are a group of progressive, invariably fatal, conditions that are associated with prions and affect the brain (encephalopathies) and nervous system of many animals, including humans, cattle, and sheep.
Poliomyelitis
Poliomyelitis, commonly shortened to polio, is an infectious disease caused by the poliovirus. In about 0.5 percent of cases, it moves from the gut to affect the central nervous system and there is muscle weakness resulting in a flaccid paralysis. This can occur over a few hours to a few days.
PNS Infections and Inflmmation
Multiple Sclerosis
MS is a demyelinating disease where myelin of the central nervous system is destroted by the body. There is then periods of restoration as the body repaires the damaged areas.
Demyelination occurs in:
- (i)White matter of the brain particularlyvthe periventricular areas, optic nerve or optic chiasm.
- (ii) Brain stem and cerebellum.
- (iii) The spinal cord usually the lateral and posterior columns.
- (iv) Some areas of grey matter.
Acute demyelination results in plaques. Plaques are the hallmark of MS and are defined areas of demyelination. The are variable in size. They are discrete, with smooth rounded edges and tend to accumulate. They are usually sclerotic.
The position of the plaque determines the symptoms observed eg plaques at the dorsal horn result in sensory loss in the area subserved by the root. Plaques occurring in the ventral horn lead to loss of motor control
The plaques cause sclerotic myelin, inflammatory cells and oedema which resolves thereby reducing symptoms. Oligodendrocytes diminish in size and there is an increase in the presence of proteolytic enzymes, macrophages, lymphocytes and plasma cells.
Remyelination can occur if the restoration phase occurs before the oligodendrocytes die.
Clinical Features
- Unilateral vision loos (optic nerve)
- Diplopia (double vision)
- Altered gait and hand movements
- Extremity and sensory loss
