Neurology

Lesions in the CNSCerebral Hemisphere* (signs opposite to side of lesion)   Hemiparesis with hyperactive deep tendon reflexes, spasticity, and Babinski sign   Hemisensory loss   Homonymous hemianopia   Partial seizures   Aphasia, hemi-inattention, and dementia   Pseudobulbar palsy Basal Ganglia* (signs opposite to side of lesion)   Movement disorders: parkinsonism, athetosis, chorea, and hemiballismus   Postural instability   Rigidity Brainstem   Cranial nerve palsy with contralateral hemiparesis   Internuclear ophthalmoplegia (MLF syndrome) : impairment of adduction of affected eye   Nystagmus   Bulbar palsy: affecting the lower cranial nerves (VII-XII). A speech deficit occurs due to paralysis or    weakness of the muscles of articulation (tongue fasciculations, drooling etc) Cerebellum (signs ON the side of lesion)   Tremor on intention†   Impaired rapid alternating movements (dysdiadocho-kinesia)†   Ataxic gait   Scanning speech Spinal Cord   Paraparesis or quadriparesis   Spasticity   Sensory loss up to a “level”   Bladder, bowel, and sexual dysfunction

Bitemporal hemianopia - the two halves lost are on the outside of each eye's peripheral vision, effectively creating a central visual tunnel. Caused by lesions at the optic chiasm e.g pituitary tumours Homonymous hemianopia - the two halves lost are on the corresponding area of the visual field in both eyes, ie either the left or the right half of the visual field. Complete ones are caused by strokes (cerebral) or middle cerebral artery lesions

Lower motor neuron Reduced tendon reflex Reduced tone Flaccid paralysis weakness Wasting Fibrillations Fasciculations

Upper motor neuron Increased (brisk) tendon reflex Increased tone  Spastic paralysis weakness Positive Babinski sign sustained ankle clonus Pyramidal pattern:  - in the arms: flexors stronger- in the legs: extensors stronger

Facial weakness: LMN lesion, the patient can't wrinkle their forehead. The lesion must be either in the pons, or outside the brainstem (posterior fossa, bony canal, middle ear or outside skull). UMN lesion, the upper facial muscles are spared because of alternative pathways in the brainstem, ie the patient can wrinkle their forehead (unless there is bilateral lesion) 

Nerve root lesions:S1 Pain along the posterior aspect of the leg and buttock till sole of foot Weakness of the medial gastrocnemius muscle with impaired ankle plantar flexion Loss of ankle jerk Sensory loss over the lateral calf and foot C5 Weakness in shoulder abduction and flexion Weakness in elbow flexion Loss of biceps reflex Sensory loss over radial part of shoulder and arm

Median nerve compression (carpal tunnel) tingling, numbness, or pain in the distribution of the median nerve (the thumb, index, and middle fingers, and medial half the ring finger on the palmar aspect) pain often worse at night and causes wakening. Weakness may be noted in hand grip and opposition of the thumb.  muscle wasting of the thenar eminence Positive Phalen's test: flexing the wrist for 60 seconds causes pain or paraesthesia in the median nerve distribution.

Ulnar nerve palsy: paralysis and weakness along ulnar side of arm and fourth and fifth digits Paralysis of interossei and the medial two lumbricals causes 'claw hand' deformity, mainly seen in the ulnar fingers. wasting of the hypothenar muscles, interossei and the medial part of the thenar eminence. weakness in movement of fingers and abduction to the extended thumb against the palm. sensory loss of the dorsal and palmar aspects of the ulnar side of the hand together with 4th and 5th digits.

Radial nerve palsy wrist drop with slightly flaccid flexion of the wrist and the hand is pronated with the thumb adducted. sensory loss of dorsal aspect of the forearm from below the elbow down over the radial part of the hand  muscle weakness in the extensor muscles and supinator

Time scales: Stroke:  > 24 hours TIA: Amaurosis fugax: seconds-minutes

DefinitionsStroke: ischaemic infarction of part of the brain or from intracerebral haemorrhage.TIA: temporary inadequacy of the circulation in part of the brain (a cerebral or retinal deficit); it is transient and reversible.Amaurosis fugax: loss of vision in one eye due to a temporary lack of blood flow to the retina, usually due to occlusion of internal carotid artery

ISCHAEMIC STROKERisk factors: Hypertension. Smoking. Diabetes mellitus. Heart disease (valvular, ischaemic, atrial fibrillation). Peripheral vascular disease. Post-TIA (TIAs are associated with a high early risk of stroke). Polycythaemia vera. Carotid artery occlusion; carotid bruit. Combined oral contraceptive pill. Hyperlipidaemia. Excess alcohol. Clotting disorders. CausesIschaemic stroke: usually due to thrombus (atherosclerosis, e.g carotid arteries) or emboli (DVT, PE).  Heart emboli are particularly associated with atrial fibrillation, infective endocarditis or myocardial infarction). vasculitis, including giant cell arteritis may increase risks of clotting and brain ischaemia Hemorrhagic stroke: Hypertension is main cause of intracerebral hemorrhages subarachnoid hemorrhage (5%) trauma medications that cause increased risk of bleeding such as warfarin

Consequences of a stroke: Weakness or paresis that may affect a single extremity, one half of the body, or all 4 extremities Facial droop Monocular or binocular blindness Blurred vision or visual field deficits Dysarthria and trouble understanding speech Vertigo or ataxia Aphasia nausea, vomiting, and headache, as well as an altered level of consciousness and meningism, may indicate increased intracranial pressure and are more common with hemorrhagic strokes  Seizures are more common in hemorrhagic stroke than in the ischaemic kind.  AF and stroke:turbulent flow and stasis of blood in AF due to irregular contraction of the atria and inefficient filling and pumping, resulting in clot formation (heart emboli)

Subarachnoid hemorrhage-commonly due to bleeding from an aneurysm in the Circle of Willis, most often from a berry aneurysm.Vascular abnormalities: 85% of patients bleed from intracranial arterial berry aneurysms,  10% from a non-aneurysmal peri-mesencephalic haemorrhage  5% from other vascular abnormalities including arteriovenous malformation. Symptoms: THUNDERCLAP HEADACHE (sudden and very very severe pain) The headache is often diffuse. It usually lasts a week or two. Other features include: Vomiting, Seizures, which occur in only about 7% Signs: - reduced level of consciousness (2 out of 3), with half in coma -intraocular haemorrhages in around 15%  - focal neurological signs like a stroke Meningism: headache, neck ache and back ache Kernig's sign: pain on extension of the knee when thigh is bent at the hip and knee at 90 degree  stiff neck on examination (nuchal rigidity) photophobia Brudzinski sign: forced flexion of the neck elicits a reflex flexion of the hips Complications:-cardiac arrest-cerebral ischaemia-hydrocephalus-epilepsy-anosmia

Subdural hemorrhageCauses: Bleeding from a damaged cortical artery. Bleeding from an underlying parenchymal injury. Tearing of bridging veins from the cortex to one of the draining venous sinuses. Blunt head trauma is the usual mechanism of injury but spontaneous SDH can arise as a consequence of clotting disorder, arteriovenous malformations/aneurysms or other conditions.At-risk groups: Infants: In the infant brain, SDHs are caused by tearing of the bridging veins in the subdural space and may result in significant brain injury.  The elderly: Cerebral atrophy causing tension on the veins, which may also be weaker and more susceptible to injury as a consequence of age. (Chronic subdural haematoma is more common in this age group) Alcoholics: higher risk of thrombocytopenia, prolonged bleeding times and blunt head trauma. Alcoholism also causes cerebral atrophy which can put tension on the bridging veins People on anticoagulation treatment: (aspirin or warfarin)  Presentation of chronic subdural haemorrhage: Usually presents about 2-3 weeks following the provoking trauma. Symptoms tend to be gradually progressive. There is often a history of anorexia, nausea and/or vomiting. Gradually evolving neurological deficit such as focal limb weakness, speech difficulties, increasing drowsiness/confusion or personality changes. accompanying and progressive headache papilloedema, bradycardia and hypertension associated with raised intracranial pressure. reduced consciousness level

MENINGO-ENCEPHALITIS-inflammation of the brain and meninges (viral or bacterial causes)Presentation: triad of fever, headache, and altered mental status. meningism: fever, headache, neck stiffness, vomiting, photophobia altered consciousness: confusion, drowsiness, seizures and coma. psychiatric symptoms begin with a flu-like illness or with a headache pyrexia symptoms of increased intracranial pressure: severe headache, vertigo, nausea, convulsions and mental confusion.  Epilepsy, focal neurological signs and cognitive impairment may develop

Meningitis rash:Petechial rash that is non-blanching on pressure, in septicaemia it is recent and changing visibly

Complications: Early complications - seizures, raised intracranial pressure, cerebral venous or sagittal sinus thrombosis, and hydrocephalus. In severe fulminant meningococcaemia - disseminated intravascular coagulation, adrenal haemorrhage and adrenal failure  Circulatory collapse and impaired renal and pulmonary function also occur. Late complications: communicating hydrocephalus, deafness (1-10% cases) which is usually irreversible.  Amputations and abnormal bone growth due to necrosis  Skin complications (including scarring from necrosis). Psychosocial problems. Neurological and developmental problems. Septic complications: septic arthritis, purulent pericarditis, endophthalmitis, pneumonia. Immune-complex complications, eg arthritis and pericarditis

CNS and Motor system

cerebrovascular events

hemorrhages

CNS infection