Neurology

Common causes of damage to FCP

Trauma e.g. surgery or facial injury

Acoustic neuroma (non cancerous tuma)

Motor Neurons Disease (most common for SLTs)

- Mixed damage of lower motor neurons and upper motor neurons

Cranial nerves associated with speech and swallowing

V Trigeminal

VII Facial

IX Glossopharyngeal

X Vagus

XII Hypoglossal

Other cranial nerves, significant but not vital, for eating and drinking

I Olfactory (smell)

II Optics (food looking attractive)

XI Accessory (Keeping head upright)

V Trigeminal

Sensory and Motor -

S= Facial, nasal and oral mucosa M= muscles of mastication

VII Facial

sensory and motor,

S=Anterior 2/3rd of tongue (taste)

M= lip and buccal tension, muscles of the lower face (lower branch)

IX Glossopharyngeal

Sensory and Motor.

S= Posterior 1/3rd of tongue

M= swallow reflex, elevation of pharynx, gag reflex

X Vagus

Sensory and Motor.

S= Airway protection and coughing

M= Soft palate, palatoglossus (extrinsic tongue muscle), velum elevation, closure of VFs, oesophagus

XII Hypoglossal

Just Motor - All intrinsic muscles of the tongue, and all extrinsic (beside palatoglossus)

V, VII IX, X, XII Cranial nerves have there origin in ...

the pons (V-VII) or medulla (IX-XII)

All part of the hindbrain

"Swallow centre" in the brain stem

nucleus tractus solitarius

AND

Nucleus ambiguous

Primary motor cortex and primary somatosensory cortex located at...

Precentral gyrus (motor)

Postcentral gyrus (somatosensory)

V, VII (upper), IX, X are innervated:

VII lower and XII are innervated

Bilaterally

VII Facial lower branch and XII Hypglossal are contralaterally innervated

If there is unilateral cortical damage, CN V, VII (upper), IX, X will be...

Okay - The non effected side of the cortex will need a bit of time, but will eventually be able to pick up the slack for the other side.

If there is cortical damage to VII (lower) or XII there would be...

Hemiplegia, contralateral to the side of the lesion as these cranial nerves are unilateral.

Strokes will effect these CN the most. Hence stroke victims often have drooped faces, swallowing and tongue difficulties.

Damage to final common pathway/lower motor neurons (LMNs)

Flaccidity/reduced tone

Flaccid Dysarthria

Fasciculations (twitching)

Atrophy

LMN damage

hypotonia/flaccidity/atrophy

UMN damage

hypertonia/spasticity

Speech motor system:

1) final common pathway

2) direct activation pathway,

3) indirect activation pathway,

4) control circuits

5) Motor programmer

1. Oral Preparatory Phase

when food is manipulated in the mouth and masticated if necessary, reducing it to a consistency ready for swallow

CN I/II prepare for eating. Smell, look.

Afferent nerves send information about consistency of food (V, VII, IX) to sensory cortex. Tongue muscle send taste (VII, IX) information. Salivation triggered (IX)

Efferent nerves control lip seal (VII), mastication (V)

2. Oral phase

Lip seal. Buccal engagement. Anterior to posterior "stripping".

Afferent informs brain of location of bolus (V, VII, IX, XII)

Efferent buccal musculature (VII) engaged. Anterior-posterior stripping (X, XII) of bolus to pharynx.

3. Pharyngeal stage

Swallow triggered when bolus reaches faucial arches. Velum elevates. Larynx elevates. VF and epiglottis close. Cricopharyngeal sphincter opens. Pharyngeal constrictors innervated.

Afferent - all relay somatosensory information which dictates autonomic and motor controls.

Efferent - Velum elevates (X), larynx elevated by complex movements (V, VII, XII), VF/Epiglottis close (X).

4. Oesophageal phase

Stage begins once bolus has gone through the cricopharyngeal sphincter.

Pushed down sequentially through contractions of oesophagus. Innervated by Glossopharyngeal and Vagus (IX, X)

Faucial arches

opening of oropharynx by soft palate and base of tongue. Triggers swallow when bolus reaches.

Four stages of swallowing

1. oral preparatory,

2. oral,

3. pharyngeal,

4. oesophageal

1. Final Common Pathway

Lower motor neurons. Part of the PNS, comprises lower motor neuron system in the form of cranial nerves

2. Direct activation pathway

Upper motor neurons.

Sometimes referred to as pyramidal tract.

Part of the descending tract (Brain-Spinal cord)

Damage to direct activation pathway...

Increased tone/spasticity

Weakness

Dysarthria

Bilateral damage = spastic dysarthria

Unilateral damage = upper motor neuron dysarthria (milder form)

3. Indirect activation pathway

Upper motor neurons.

Sometimes called extra-pyramidal tract.

Functions for speech poorly understood.

Damage to indirect activation pathway...

Spasticity and hyperreflexia.

Bilateral damage = spastic dysarthria

Unilateral damage= upper motor neuron dysarthria (milder form)

4. Subcortical structures

basal ganglia, cerebellum (important to SLTs)

Others less important to us:

thalamus, hypothalamus, hippocampus, amygdala

Basal ganglia and speech

Exact function of individual components of BG not understood well.

As a group they help regulate posture, muscle tone, static muscle contraction, velocity, amplitude and initiation of movement.

Damage to basal ganglia

Presentation:

- Hypokinesia

- Hyperkinesia

- Dysarthria

Causes

- Parkinson's Disease PD (Hypokinetic Dysarthria)

- Huntington's Disease HD (Hyperkinetic Dysarthria)

hypokinetic vs hyperkinetic

damage to basal ganglia effecting movement.

Hypokinetic = reduced movement

Hyperkinetic = involuntary excess movement

Cerebellum and speech

Posture and movement. Interacts with direct and indirect activation pathway to coordinate muscle groups for motor speech.

nystagmus

Involuntary rapid eye movements

intention tremor

involuntary trembling when an individual attempts a voluntary movement

Dysmetria

inability to control the distance, power, and speed of a muscular action

hypotonia

reduced muscle tone or tension

Damage to cerebellum

Coordination issues.

Dysmetria - Inability to control distance, speed and range of motion necessary to perform coordinated movements Nystagmus - Repetitive and involuntary movement of eyes

Intention tremor - Tremor during intense activities such as handwriting or speaking

Hypotonia - Decreased muscle tone

Ataxic dysarthria - distinctive motor speech disorder associated with damage to the cerebellar control circuit

Ataxic Dysarthria

Results from damage to cerebellar system. Articulatory & prosodic (rhythm) problems

5. Motor programming

Developing a plan to organise and coordinate speech movements.

Localisation - language dominant hemisphere, sensory and motor cortices, premotor cortex

Damage to motor programming stage

Apraxia of Speech (AOS) - As the main Motor Speech Disorder MSD

- Left/dominant hemisphere, near Brocas area.

- Someone with Brocas Type Aphasia may also have an companying MSD in form of AOS

perisylvian fissure

Peri=about or around

Therefore around the sylvian fissure.

Divides Broca's and Wernicke's areas

Dysarthria

neuromuscular speech disorder upper/lower MN.

Consistent errors, weakness, spasticity, or involuntary movements.

apraxia of speech

impairment in the ability to program movements caused by CNS damage.

Not necessarily weak, flaccid or spastic.

Inconsistent errors

May be able to produce spontaneous speech, but struggle when planned.

Groping for a sound they cant make.

Aphasia

impairment of language, not just articulation. usually caused by left hemisphere damage.

middle cerebral artery (especially left)- importance for speech and language?

supplies the left middle brain where language and speech areas are.

Strokes involving the MCA - likely impact communication

progressive neurological disorders

Deteriorates over time e.g. MND, Alzheimer's, Parkinson's

Non-progressive neurological disorder

Will either improve slightly/completely, or remain static in effect.

cerebrovascular accident CVA

stroke, lack of blood supply to the brain causing brain damage.

Occupy 20% of acute hospitral beds.

4th largest cause of death in the UK.

Risk factors for cerebrovascular accident

Hypertension (high BP)

Heart disease (including myocardial infarction - heart attacks) and atrial fibrillation (irregular and abnormally fast heart rate)

Family history

Cholesterol

infarct

Area of dead tissue after a lack of blood supply

myocardial infarction

heart attack

atrial fibrillation

irregular and abnormally fast heart rate

Ischaemic CVA

Most common CVA - 85%.

blood vessel occlusion from atherosclerotic thrombus or embolus

haemorrhagic CVA

Less common CVA - 15%.

bursting of blood vessels

embolism

the sudden blockage of a blood vessel by an embolus. Forms elsewhere then travels to the brain

thrombosis

abnormal condition of a blood clot - forms inside the brain and blocks there

Circle of Willis

A circle of arteries at the base of the brain that supply blood to the brain

Provide a fail safe for ischaemic strokes, if one part blocks it can be reached by other wys.

Circle of Willis inflowing arteries...

Internal Carotid Artery

Vertebral Artery

Circle of Willis outflowing arteries...

Anterior Cerebral Artery (ACA)

Middle Cerebral Artery (MCA)

Posterior Cerebral Artery (PCA)

Blood supply to lateral surface of brain

Mostly middle cerebral artery, with ACA to the anterior and PCA to the posterior

Blood supply to medial part of brain

mostly ACA, with PCA to posterior

Blood supply to brain when looking axially

ACA to anterior, MCA to sides, PCA to posterior

Four types of Oxford Classification System strokes and why is it used

1- Total Anterior Circulation Syndrome (TACS)

2- Partial Anterior Circulation Syndrome (PACS)

3- Posterior Circulation Syndrome (POCS)

4- Lacunar Stroke (LACS)

Intends to classify strokes without jargon. Accessible to pts and clinicians.

Based on idea that site and size of lesion will influence presentation and prognosis.

anopia

blindness

homonymous hemianopia

The loss of the right or left half of the field of vision in both eyes. Due to leision at the optic tract/visual cortex of the brain (as left hemisphere of brain controls visual hemfield for right of both eyes and visa versa)

1- Total Anterior Circulatory Stroke (TACS)

Has to present with all 3:

1- Unilateral weakness and/or sensory impairment of face arm and leg

2- Homonymous hemianopia

3- Higher cerebral dysfunction (e.g. aphasia)

MCA and ACA arteries effected.

Prognosis:

- 56% die

- 39% dependent

-4% independent

2- Partial Anterior Circulatory Stroke (PACS)

Has to present with 2 of the 3 features:

1- Unilateral weakness and/or sensory impairment of face arm and leg

2- Homonymous hemianopia

3- Higher cerebral dysfunction (e.g. aphasia)

Only part of ACA effected

Prognosis - 10% don't survive

34% dependent

55% independent

3. Posterior Circulation Stroke (POCS)

One of the following:

1- Cranial nerve palsy and a contralateral motor/sensory deficit

2- Bilateral motor/sensory deficit

3- Conjugate eye movement disorder (e.g. horizontal gaze palsy)

3- Cerebellar dysfunction (e.g. vertigo, nystagmus, ataxia)

5- Isolated homonymous hemianopia

Damage to posterior circulation e.g. cerebellum and brainstem

Prognosis:

14% die

18% dependent

68% independent

4. Lacunar Stroke (LACS)

One of the following:

1- Pure sensory stroke

2- Pure motor stroke

3- Sensori-motor stroke

4- Ataxic hemiparesis

Subcortical stroke that occurs secondary to small vessel disease. No higher cerebral dysfunciton (e.g. aphasia)

Prognosis:

7% die

26% dependent

66% independent

computed tomography (CT)

brain-imaging method using computer-controlled X-rays of the brain

- Easily available

- Quick to complete

- Good for bone and fresh blood

magentic resonance imaging (MRI)

magnetic waves produce images of organs and tissues in all three planes of the body

- More expensive (less availability)

- Takes longer

- Better for brain tissues

- 3 planes

Symptoms for stroke

Hemiplegia, dysarthria, dysphasia, hemianopia, aphasia

anxiety

neglect

agnosia

balance impairments

anticoagulant

prevents blood clotting prior to a stroke e.g. aspirin (not to be used during a stroke)

Used for haemorrhagic strokes

thrombolysis

destruction of a blood clot by breaking it down and dispersing

thrombectomy

surgical physical removal of a blood clot

Traumatic Brain Injury (TBI)

a blow to the head or a penetrating head injury that damages the brain

Half of all deaths in under 40s are caused by TBI

TBI- first injury

- Initial damage to the brain that occurs at the time of damage

Closed

- Skull intact

- Brain not exposed

Open

- Skull integrity

- Brain exposed

Crush

- Head crushed

TBI second injury

- Can occur at dif times after minutes or days/weeks/months

- Lack of oxygen

- Bruising

- Raised intracranial pressure

- Infection

- Formation of blood clots

contusions

bruises

Haematoma

Localised congealed bleeding outside of blood vessels

haemorrhage

excessive bleeding involving blood vessels

Focal Damage (TBI)

- Contusions (may occur opposite side of brain - ricochet)

- intracranial haematoma

- sub dural/extra dural haematomas

- intra-ventricular haemorrhages

intra-ventricular haemorrhages

bleeding into the ventricles of the brain

Brain meniges

layers of protection over the brain

Different layers of meninges

Skin -- > Cranium --> Dura Mater --> Arachnoid Mater --> Pia mater --> Brain

dura mater (hard mother)

thick, outermost layer of the meninges surrounding and protecting the brain and spinal cord

arachnoid mater

weblike middle layer of the three meninges. No blood vessels or nerves.

pia mater

thin, delicate inner most membrane of the meninges with many tiny blood vessels.

TBI symptoms

aphasia, AOS, dysarthria, initial mutism, confused language, naming difficulties, difficulty initiating conversation, reduced word fluency, lack of turn taking, imprecise language, reading and writing problems, comprehension auditory deficits

Treating TBI

reducing secondary complications, airway patent, oxygen therapy, ventilation, surgery, anticonvulsants for epilepsy, monitor closely, treating intercranial pressure, rehabiliation

cerbrovascular accident CVA

aka stroke; ischemic or hemorrhagic; brain tissue dies

neurodegenrative disease

progressive decline in the structure, activity and function of CNS or PNS.

idiopathic

unknown cause

Parkinson's disease aetiology

-Progressive disease of the CNS, mostly effecting basal ganglia

- Loss of dopamine producing neurons in the midbrain

- Idiopathic

basal ganglia

a set of subcortical structures that work together to regulate motor function.

Requires neurotransmitter dopamine

PD characteristics

-Resting tremor - sometimes "Pill rolling"

- Rigidity/hypertonia

-Hypokinesia - leads to reduced facial expressions

- Hypokinetic dysarthria

- Dysphagia

- Language/cognitive issues

- PDD/DLB

Neuropsychiatric symptoms of PD

-Dementia (Parkinson's Disease Dementia/DLB)

- 30% of PD will progress to dementia

- Memory/cognitive changes

- Depression

- Anxiety

- Hallucinations

Hypokinetic Dysarthria

Results from damage to basal ganglia (e.g. PD)

- Imprecise consonants

- Monopitch/monoloudness

- Neurogenic dysfluency (repetition of utterances/words)

- Reduced vital capacity of lungs