Oxford handbook of neurology free download

Inferior Middle cerebellar cerebellar peduncle peduncle. Medial Vestibular Nucleus longitudinal Abducens nucleus reticularis fasiculus nucleus pontine c Ventral tegmental area Mammillary body Oculomotor nerve III Frontopontine tract Red nucleus Corticonuclear tract Brachium Corticospinal tract conjuctivum Substantia nigra pars reticulata Substantia nigra pars compacta Lemniscal system Parietotemporal pontine Oculomotor nucleus tract.

Dorsal raphe nucleus Nucleus reticularis Cerebral aqueduct Intercollicular nucleus Periaqueductal grey. Posterior cerebral a.

PCA Posterior choroidal a. Collicular a. Medial superior cerebellar a. Lateral superior cerebellar a. Basilar a. Pontine a. Anterior inferior cerebellar a. AICA Posterior inferior cerebellar a. PICA Vertebral a. Reproduced from P. Gates The rule of 4 of the brainstem: a simplified method for understanding brainstem anatomy and brainstem vascular syndromes for the non-neurologist.

Dorsal columns. Fasciculus Fasciculus Lateral corticospinal tract cuneatus gracilis. Rubrospinal tract Neuroanatomy. Somatotopic arrangement of motor. Philadelphia, units in anterior horn shown in spinal grey matter. Arrangement of tracts: C, cervical; T, thoracic; L, lumbar; S, sacral. Chapter 3 Presentation More common in those with mental handicaps or structural lesions, espe- cially children.

Complications and management See Table 3. Table 3. IV lorazepam - 4 mg 0. IV thiamine - mg slow infusion e. EFNS guideline on the management of status epilep- ticus in adults. In the early stages of an acute myelopathy due to trauma, an intraspinal haemorrhage or myelitis due to inflammatory or infectious causes, clinical signs may resemble those of a peripheral rather than a central disorder.

For example, sudden-onset paraparesis is most likely to be due to a vascular insult to the spinal cord such as anterior spinal artery ASA thrombosis. Key finding is depressed or absent reflexes which will also be found in weakness due to secondary hypokalaemia. Spinal cord compression without pain and a sensory level is unusual. Persistent hypertension and tachycardia in association with pure motor weakness occurs in porphyria.

Differential diagnosis See Table 3. Acute neuromuscular weakness EMG studies show decrement. Reflexes intact Single fibre—jitter Lambert—Eaton Variable muscle weakness. Voltage-gated calcium-channel syndrome Ocular muscles spared. Short exercise EMG; mutation periodic paralysis Duration: hours to days. May be first episode of demyelination or viral, e. In cases preceded by C. By definition nadir is reached in 4 weeks.

If i consider HIV infection seroconversion , Lyme disease, or malignant infiltration e. Similar efficacy to plasma exchange PE. Dose: 0. Four exchanges sufficient for moderate to severe disease. In mild disease able to stand but not run , two exchanges may be adequate. Regular monitoring of vital capacity VC , not peak flow, is essential.

By the time O2 saturation or the PO2 falls, it is too late. ECG monitoring essential on severely affected patients at least until they are recovering. Amitriptyline should be avoided especially in the early stages because of its potential cardiac side effects.

Lancet Neurol. Note: first ever episode—exclude SAH. A first episode of headache cannot be classified as tension-type headache IHS criteria for diagnosis requires at least 9 similar episodes or migraine 4 previous episodes required for diagnosis without aura. Acute headache thunderclap headache Investigations All patients should have a CT scan and, if that is negative, a lumbar puncture.

Expertise in reading CT scans is essential. If there are a lot more white cells consider meningitis complicated by a traumatic tap. In SAH protein is usually elevated. After 3—5 days, polymorphs and lymphocytes. Clinical presentation Clinical severity varies widely. May occur during strenuous activity such as sexual intercourse. Associated with vomiting.

See Tables 3. Management See Fig. Subarachnoid haemorrhage SAH Strict bed rest until diagnosis determined, elevate head of bed to 45 degrees.

Prescribe adequate analgesia IV opiates if necessary and anti-emetics. Increased lethargy 3. Seizures Urgent CT Head to exclude hydrocephalus or re-bleed Aneurysm present Neurosurgical clipping or endovascular coiling depending on aneurysmal site, clinical condition, comorbities, local practice. Appears most useful around the time of endovascular coil or neurosurgical clip interventions, but the effects are probably not sustained.

However, emergency treatment is only advocated in those with large ICHs secondary to middle cerebral artery aneurysms. Has a typically benign course. Patient may have headaches for several weeks but no further haemorrhages. Small risk for development of hydrocephalus. Part 2: Surgical results. A small amount of sulcal blood is also shown small black arrow. Note the mild degree of communicating hydrocephalus. Note the surrounding bilateral inferior frontal parenchymal low attenuation representing early ischaemia.

There is marked vasospasm and slower flow in the proximal left anterior cerebral artery black arrowheads with reduced opacification of the distal vessels in the ACA territory. Imaging of SAH: examples Communicating hydrocephalus.

The distri- bution is suggestive of a right MCA aneurysm which is shown on subsequent MRI as a rounded signal flow void black arrow. Figure 3. The fundus of the large PCom artery aneurysm white arrowheads is directed postero- laterally and the neck arises from the communicating segment of the right internal carotid artery white arrows. This is confirmed on digital subtraction angiogram following selective catheterization of the right internal carotid artery.

In b the aneurysm open black arrowheads arises via a relatively narrow neck black arrow from the communicating segment of the right ICA. Note contrast within the right posterior cerebral artery closed black arrowheads indicating the presence of a prominent persistent posterior communicating artery. Figures 3. The aneurysm is completely excluded and the posterior communicating artery is preserved with continued flow within the posterior cerebral artery black arrowheads in d.

Acute focal neurological syndromes In patients who present with acute focal neurological deficit, the history and examination should point to the site of pathology and the possible patho- logical mechanism s. Acute focal neurological syndromes Management of acute ischaemic stroke See Table 3. Rapid Screening: Potential candidate for thrombolysis?

Time of onset known? Migraine, seizures. Refer to spontaneous ICH. NO max. Transfer to hyperacute stoke unit if appropriate Secondary prevention.

More common in patients on ACE inhibitors. Management of acute ischaemic stroke Record performance in each category after each subscale exam. Do not go back and change scores. Follow directions provided for each exam technique. Scores should reflect what the patient does, not what the clinician thinks the patient can do.

The clinician should record answers while administering the exam and work quickly. Except where indicated, the patient should not be coached i. It is important that only the initial answer be graded and that the examiner not "help" the patient with verbal or non-verbal cues.

Credit is given if an unequivocal attempt is made but not completed due to weakness. Patients with trauma, amputation, or other physical impediments should be given suitable one-step commands. Only the first attempt is scored.

Best Gaze: Only horizontal eye movements will be tested. If the patient has but forced deviation or total gaze paresis is not present. If a patient the oculocephalic maneuver. Gaze is testable in all aphasic patients. Patients with ocular trauma, bandages, pre-existing blindness, or other disorder of visual acuity or fields should be tested with reflexive movements, and a choice made by the investigator.

Establishing eye contact and then moving about the patient from side to side will occasionally clarify the presence of a partial gaze palsy. If patient is blind from any cause, score 3. Double simultaneous stimulation is performed at this point. Each if cued 90 or 45 degrees, drifts down to bed, but has limb is tested in turn, beginning with the non-paretic arm.

Instructions Scale Definition Score 6. The aphasic patient not hit bed. Each limb is tested in turn, beginning but has some effort against gravity. Right Leg. Test with eyes open. Only in the case of amputation or joint fusion, the examiner should record the score as untestable UN , and clearly write the explanation for this choice. In case of blindness, test by having the patient touch nose from extended arm position.

Only sensory loss attributed to stroke is scored as less sharp or is dull on the affected side; or there is a loss abnormal and the examiner should test as many body areas of superficial pain with pinprick, but patient is aware of arms [not hands], legs, trunk, face as needed to accurately being touched. The patient with brainstem stroke who has bilateral loss of sensation is scored 2. If the patient does not respond and is quadriplegic, score 2.

For this scale item, the patient is fluency or facility of comprehension, without significant asked to describe what is happening in the attached picture, limitation on ideas expressed or form of expression. Comprehension is judged makes conversation about provided materials difficult or from responses here, as well as to all of the commands in the impossible.

For example, in conversation about provided preceding general neurological exam. The examiner guessing by the listener. Range of information that must choose a score for the patient with stupor or limited can be exchanged is limited; listener carries burden of cooperation, but a score of 3 should be used only if the communication.

Examiner cannot identify materials patient is mute and follows no one-step commands. If words and, at worst, can be understood with some the patient has severe aphasia, the clarity of articulation difficulty. Do not tell the patient why he or she is being tested.

If the patient has a severe visual loss preventing extinction to bilateral simultaneous stimulation in one of the visual double simultaneous stimulation, and the cutaneous sensory modalities. The presence of visual spatial neglect or only one side of space. Since the abnormality is scored only if present, the item is never untestable. Management of acute stroke. National clinical guideline for stroke, 4th edition. London: Royal College of Physicians.

Diagnosis and management of transient ischaemic attack and ischaemic stroke in the acute phase. NICE Stroke: diagnosis and initial management of stroke and transient ischaemic attack.

Spontaneous intracranial haemorrhage ICH Recent STICH trials suggest no benefit for surgery versus conservative management in the early stages. Infratentorial haematomas are special cases—may warrant surgical intervention for evacuation or shunt insertion for hydrocephalus. Spontaneous intracerebral haem- orrhage: a clinical review. Imaging of ICH: examples Figure 3. Note the small rim of surrounding low attenuation and associated mass effect with ipsilateral sulcal effacement. Imaging of ICH: examples There is little associated mass effect.

Note the large draining vein entering the vein of Galen white arrow. Bilateral posteriorly dis- tributed peripheral haemosiderin staining indicates previous lobar haemor- rhage white arrows , with multiple widely distributed foci of haemosiderin in both cerebral hemispheres black arrowheads. Note the absence of sur- rounding white matter signal change, suggesting no recent extralesional haemorrhage.

Epidemiology Common in general medicine, especially in the elderly. Pathophysiology Not well understood, but evidence for cholinergic underactivity and dopa- minergic overactivity. Delirium However, d activity is as common, but is under-recognized and diagnosed as depressed or tired.

Look for signs of infection, dehydration, constipation. Look at drug chart carefully. Delirium in elderly people. Initial assessment according to ATLS protocols. Avoid hypoxia O2 sat. Assessment of conscious level using the Glasgow Coma Scale see Table 3.

If GCS not depressed, detailed assessment of limb power, sensory assessment, cranial nerve function including pupillary responses, corneal reflexes, gag and cough reflexes.

Observe respiratory pattern and rate. Check pulse and BP. Check for scalp lacerations, rhinorrhoea, otorrhoea, haemotympanum, and extracranial injuries. If possible determine retrograde and anterograde amnesia. Head injuries are strongly associated with cervical injury. Head injury HI Management b See also Chapter 7.

Regular neurological observation to detect any deterioration. Corticosteroids have no place in the management of head injuries. Referral to a neurosurgical centre and image transfer if possible of: all moderate to severe HI, abnormal CT scan, depressed GCS with normal CT scan, all penetrating injuries, uncertain CT findings due to lack of expertise. Secondary phase management Respiratory management Aim for target arterial CO2 of 4—4.

If prolonged ventilation, consider tracheostomy. ICP is monitored via an intraventricular or intracerebral bolt placed close to the most affected region. Management of specific head injuries May cross sutures and extend into the interhemispheric fissure and over tentorium. Hyperacute or active bleeding can be low density. Imaging CT: low density or isodense mass that may be loculated. Most common sites are the anterior-inferior temporal and frontal lobes. Angiography is mandatory for deep penetrating injuries.

Imaging of head injuries: examples Figure 3. There is an extensive underlying parenchymal contusion com- prising low-attenuation components closed white arrowheads and central haemorrhagic change open white arrows. There is an associated mass effect with ipsilateral sulcal and ventricular effacement and minor distortion of the midline. Note also the small right frontal extradural haematoma black arrow. Note also smaller foci of parenchymal haemorrhage in the occipital lobe bilaterally closed white arrowheads , intraventricular and suba- rachnoid blood black arrows , and an extensive tentorial subdural haema- toma black arrowheads.

Imaging of head injuries: examples Large acute subdural haematoma with crescentic configuration overlying left cerebral convexity with minor extension into interhemispheric fissure is shown in Fig. There is marked associated mass effect with ipsilateral sulcal and ventricular effacement and severe midline shift.

Note the indirect site of impact over right parietal bone white arrow. In contrast, note CSF clefts black arrowheads associated with bifrontal extradural haematoma in b which has a biconvex configuration. Frontal horns of the lateral ventricles are grossly effaced.

The large subdural haematoma over the left cerebral convexity and extending into the interhemispheric fissure shown in Fig. The left frontal chronic subdural haematoma shown in Fig. There is also a minor alteration in the configuration of the left frontal horn due to mass effect. The hyperdense components represent acute haemor- rhage; the low-attenuation material reflects active bleeding and unclotted oxygenated blood.

In Fig. Incomplete lesions including sacral sparing, i. Instability refers to the increased likelihood of further spinal damage. Resuscitation and airway protection. Immobilization of the neck and log rolling during assessment and resuscitation. Treatment of life-threatening injuries and bleeding. Urinary catheter. Full neurological examination to determine level and completeness lesion. Note any autonomic dysfunction, e.

Fracture in two places is typical. Usually fatal. Spinal injuries Clinical features Rarely have a neurological deficit as the spinal canal is wide and fragments burst outwards. C2 fractures Odontoid peg fractures Frequently associated with multiple injuries with high force impact. Unusual in type 3 fractures. Due to bilateral fractures of pars articularis of C2. Clinical features High proportion have a significant neurological deficit. Avoid secondary complications and maximize rehabilitation.

If unstable, fractures are treated with prolonged bed rest or internal fixation to allow early rehabilitation. All others require internal fixation and fusion. Imaging spinal injuries: examples Figure 3.

There is slight anterior subluxation of C2 upon C3. Imaging spinal injuries: examples There is a shallow epidural haematoma posterior to the C4 vertebral body open white arrow which has elevated and posteriorly displaced the dura black arrowheads. The spinal cord is distorted and displaced, although no cord contusion is evident at this stage. Note the shallow haematoma in the pre-vertebral soft tissue compartment open white arrowheads.

Discontinuity of the anterior longitudinal ligament indicates probable injury b closed white arrow. Dynamic plain X-rays demonstrate marked instability at the atlanto-axial joint as a result of a fracture through the odontoid peg Fig. Further evaluation with MRI Fig. Intramedullary signal change and spinal cord volume loss black arrow are in keeping with myelomalacia and long-standing instability and intermittent spinal cord compression. Meningitis See Table 3. Vaccination against Haemophilus influenzae type b and group C meningococcus has had significant impact.

Meningitis See Table 3. Management Choice of antibiotic Choice of antibiotic depends on age of patient and any other associated features, e. CT or LP should not delay first dose of antibiotic. Patient should be managed on ITU. Give mannitol 0. May require sedation, intubation, and ventila- tion to reduce PCO2 and controlled hypothermia.

If seizures continue, treat as for status epilepticus. Corticosteroids Shown to reduce morbidity in adults specifically in S. Bacterial meningitis considered. Spinal cord disorders See Fig. Tumour Clinically pinprick most useful in localizing. Contralateral spinothalamic loss Cord pain, temperature compression. Areflexic, flaccid paraparesis Anterior cord 2. Pain and temperature loss with dorsal column artery occlusion proprioception and light touch preservation. Diffuse weakness, atrophy, and fasciculations Spinal muscular Anterior horn cell 2.

Reduced tone atrophy syndrome syndromes 3. Sensory symptoms absent. Combined 1. Preservation of sphincters. Dorsal column loss proprioception, vibration Subacute Posterolateral combined 2. UMN signs reflexes, plantars, weakness degeneration of column syndrome 3. Preservation of pain and temperature the spinal cord.

Dorsal column loss proprioception, vibration Posterior column 2. Sacral cord and 1. Minor motor involvement. Cauda equina spinal 1. Spinal cord disorders Raised intracranial pressure See Table 3.

May cause may be small masses. May compression of Bilateral Babinski. Use transiently if signs of brainstem herniation appear. Acute encephalitis including limbic encephalitis Recent issues in herpes simplex encephalitis. Schott J An effective immunotherapy regimen for VGKC antibody positive limbic encephalitis.

Consider transvaginal US. Other tumours: SCC lung, testicular teratoma. Anti-NMDA receptor encephalitis Chapter 4 Loss of consciousness A common problem. May need to contact eyewitnesses by telephone. Time will make the diagnosis clear. Avoid trials of anticonvulsants. Tell patient it is their duty to inform the DVLA.

Loss of consciousness Diagnosis See Table 4. The eyewitness account will help make the diagnosis. Must be reported by experienced personnel. If necessary, a prolonged cardiomemo reveal device ; echocardiogram for cardiac syncope.

Sensitive for syncopal tendencies. Note: frontal lobe epileptic seizures may appear normal even on ictal EEG. Table 4. Acute vertigo Vertigo is the illusion of rotation caused by asymmetry of neural activity between the right and left vestibular nuclei. Bilateral damage does not cause vertigo. Acute vertigo with no other signs or symptoms is unlikely to be due to vertebrobasilar ischaemia. Clinical presentation is similar to that of vestibular neuritis but usually occurs in older patients with risk factors for stroke, such as diabetes, hypertension, and cardiac disease e.

Diagnosis of exclusion. Clinical features Clinical presentation is with acute-onset vertigo, nausea, and vomiting. Acute vertigo At bedside, if Fresnel lenses not available, use an ophthalmoscope focused on the optic disc or the retinal blood vessels with the other eye covered.

The nystagmus should be evident in the primary position. Note that the direction of the nystagmus is inverted when viewed through the ophthalmoscope. The head impulse test A bedside test of the horizontal vestibulo-ocular reflex see Fig. The patient illustrated has a right peripheral lesion with a severe loss of right lateral semicircular canal function. It is essential that the head is turned as rapidly as possible; otherwise smooth pursuit eye movements will compensate for the head turn.

Reproduced with permission from G. Halmagyi Diagnosis and management of vertigo. Royal College of Physicians. Positive test—patient veers to side of the lesion.

Cerebellar lesion patients unable to stand unaided to do test. Does not discriminate between central and peripheral causes. Those with a central lesion are often unable to stand without support. Some may be associated with diplopia, dysarthria, or facial numbness. Differential diagnosis See Table 4. Symptoms always resolve in a few days due to vestibular compensatory mechanisms.

MRI more sensitive at detection of posterior fossa infarcts. Positive from cholesteatoma coughing or fistula test vertigo sneezing; may be and nystagmus associated with induced by pressure chronic otitis and in the external canal cholesteatoma Brainstem Abrupt onset; Spontaneous central Unilateral caloric and history of vascular nystagmus; head hypoexcitability if cerebellar disease; other impulse test positive anterior inferior infarction neurological only if root entry cerebellar artery symptoms zone involved; focal involved.

Further reading Bronstein A, Lempert T Dizziness: a practical approach to diagnosis and management. Cambridge: Cambridge University Press. Spastic paraparesis Bilateral upper motor neuron signs in the legs. A common presentation caused by a variety of disorders. Aetiology See Table 4. In cases of undiagnosed spastic paraparesis consider a trial of L-dopa for dopa-responsive dystonia.

Myelopathy but normal MRI: what to do next. May be more apparent when turning or stopping suddenly. When mild, only tandem gait may be impaired.

Postural static tremors may also occur. Macrosaccadic square-wave jerks in primary position sudden short-duration movements laterally with rapid correction. Ataxia Autosomal dominant cerebellar ataxias At least 25 spinocerebellar ataxia genes.

Ataxia in combination with any of the following—pyramidal, peripheral nerve, ophthalmoplegia, dementia. Absence of a family history does not exclude the possibility of diagnosis. Recessive ataxias See Table 4. Episodic ataxias See Table 5. Click it to start downloading this masterpiece for free.

Download Link. Thursday, January 13, All Things Medicine. Share on Facebook. Has very valuable hints and notes that you will not find in large textbooks. Is practice, utility, and necesary. The Oxford Medical Editorial congratulations, god work, excelent books. Great Book must have and Read. Neuroanatomy ; 3. Neurological emergencies ; 4. Common clinical presentations ; 5.

Neurological disorders ; 6. Neurology in medicine ; 7. Neurosurgery ; 8. Clinical neurophysiology ; 9. Show more. Show less.